Opportunity Information: Apply for RFA DK 15 025
Apply for RFA DK 15 025
- The National Institutes of Health in the food and nutrition health sector is offering a public funding opportunity titled "Mechanisms Underlying the Contribution of Type 1 Diabetes Risk Associated Variants (DP3)" and is now available to receive applicants.
- Interested and eligible applicants and submit their applications by referencing the CFDA number(s): 93.847 Diabetes, Digestive, and Kidney Diseases Extramural Research 93.855 Allergy and Infectious Diseases Research 93.856 Microbiology and Infectious Diseases Research.
- This funding opportunity was created on Jul 7, 2015 and posted on Jul 7, 2015.
- Applicants must submit their applications by Feb 17, 2016. (Agency may still review applications by suitable applicants for the remaining/unused allocated funding in 2026.)
- The funding agency has allocated a total of $15,000,000.00 to eligible and selected applicants.
- Each selected applicant is eligible to receive up to $600,000.00 in funding.
- Eligible applicants include: Small businesses Native American tribal organizations (other than Federally recognized tribal governments) Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education Public and State controlled institutions of higher education Independent school districts Special district governments City or township governments County governments For profit organizations other than small businesses Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education Public housing authorities/Indian housing authorities Others (see text field entitled Additional Information on Eligibility for clarification) State governments Private institutions of higher education Native American tribal governments (Federally recognized).
- Other Eligible Applicants include the following Alaska Native and Native Hawaiian Serving Institutions Asian American Native American Pacific Islander Serving Institutions (AANAPISISs) Eligible Agencies of the Federal Government Faith based or Community based Organizations Hispanic serving Institutions Historically Black Colleges and Universities (HBCUs) Indian/Native American Tribal Governments (Other than Federally Recognized) Non domestic (non U.S.) Entities (Foreign Organizations) Regional Organizations Tribally Controlled Colleges and Universities (TCCUs) U.S. Territory or Possession.
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Opportunity Summary:
The NIH grant opportunity "Mechanisms Underlying the Contribution of Type 1 Diabetes Risk Associated Variants (DP3)" (Funding Opportunity Number RFA-DK-15-025) supported research aimed at moving beyond statistical genetic associations and into the biology of type 1 diabetes (T1D). The core purpose was to fund projects that closely characterize genetic variation within human genomic regions that have already been linked, in a preliminary or putative way, to T1D risk, and then to perform functional follow-up studies to determine how specific variants might influence disease. In practice, this means taking regions flagged by prior genetic studies (for example, genome-wide association studies) and doing the deeper work needed to identify which exact DNA changes matter, which genes they affect, and what those genes do in relevant cell types and immune or pancreatic pathways that contribute to T1D.
A key emphasis of the FOA was that many T1D-associated regions do not point neatly to a single obvious "candidate" gene. For those loci, applicants were encouraged to do additional mapping and mechanistic studies to identify the causal gene(s) and the causal variant(s), then explain how altered gene function or gene regulation contributes to the development of T1D. The announcement explicitly framed this as a gap in the field: association signals are common, but the biological mechanisms are often unclear. By encouraging careful variant characterization and functional experimentation, the FOA aimed to produce insights that could clarify disease pathogenesis, including how immune dysregulation and beta cell biology are influenced by inherited variation.
This opportunity was a discretionary grant program using the grant funding instrument type, with activity categorized under Food and Nutrition/Health and linked to multiple CFDA numbers, including 93.847 (Diabetes, Digestive, and Kidney Diseases Extramural Research) and also 93.855 and 93.856 (allergy/infectious diseases and microbiology/infectious diseases), reflecting the immunologic and inflammatory dimensions of T1D research. Cost sharing or matching was not required, which generally lowers barriers for applicants by making budgets dependent on project needs rather than institutional matching commitments.
From a funding standpoint, the FOA listed an estimated total funding amount of $15,000,000 and an award ceiling of $600,000. While the announcement text provided here does not specify the number of awards, the combination of a total program figure and a per-award cap indicates support for multiple projects, each expected to propose a focused, mechanistically driven plan that connects specific genetic variants to functional outcomes. The posting date and creation date were July 7, 2015, with an original and current closing date of February 17, 2016, and an archive date of March 19, 2016, meaning the competition is now closed but remains relevant as a historical reference for the kinds of studies NIH prioritized in this area.
Eligibility was broad and included a wide range of organizations: public and private institutions of higher education, nonprofit organizations (including those with and without 501(c)(3) status), for-profit organizations (including small businesses and other for-profits), and numerous government entities (city or township, county, state, special district governments, independent school districts, and public housing authorities/Indian housing authorities). The eligibility section also extended to organizations serving specific communities and missions, such as HBCUs, Hispanic-serving institutions, tribally controlled colleges and universities, Alaska Native and Native Hawaiian serving institutions, AANAPISIs, faith-based or community-based organizations, U.S. territories or possessions, regional organizations, and even non-U.S. entities (foreign organizations). This wide eligibility net suggests NIH’s intent to attract a diverse set of scientific teams and institutional settings capable of conducting genetic and functional genomics research relevant to T1D.
Overall, the grant was designed for investigators who could integrate human genetics with functional biology to answer a central question: which specific DNA variants drive T1D risk, through what genes, in which cells, and by what regulatory or molecular mechanisms? The intended payoff was not simply confirming association signals, but pinpointing causal biology that could refine our understanding of T1D onset and progression and potentially inform new preventive or therapeutic directions. For applicants or readers seeking full details, the FOA pointed to the official NIH guide page (http://grants.nih.gov/grants/guide/rfa-files/RFA-DK-15-025.html) and provided NIH Office of Extramural Research webmaster contacts for access or linking issues.
FAQs: NIH RFA-DK-15-025 (DP3) - Mechanisms Underlying the Contribution of Type 1 Diabetes Risk Associated Variants
What is the name of this NIH funding opportunity?
The opportunity is titled "Mechanisms Underlying the Contribution of Type 1 Diabetes Risk Associated Variants (DP3)" and has Funding Opportunity Number (FON) RFA-DK-15-025.
What was the main purpose of this FOA?
The purpose was to support research that moves beyond statistical genetic associations and into the underlying biology of type 1 diabetes (T1D). Projects were expected to closely characterize genetic variation in human genomic regions already linked (preliminarily or putatively) to T1D risk, then perform functional follow-up studies to determine how specific variants might influence disease.
What kind of research approach did NIH want to fund under this announcement?
NIH prioritized studies that start with previously identified T1D-associated genomic regions (for example, regions flagged in prior genetic studies such as genome-wide association studies) and then do deeper mapping and mechanistic work to identify which exact DNA changes matter, which genes they affect, and what those genes do in relevant cell types and pathways.
What problem or gap in the field did this FOA target?
The FOA emphasized that many T1D association signals are known, but the biological mechanisms behind them are often unclear. In particular, many associated regions do not point neatly to a single obvious candidate gene. The gap it aimed to address was translating association signals into causal variants, causal genes, and clear mechanistic explanations for disease risk.
What does "moving beyond association" mean in the context of this FOA?
It means not stopping at a statistical link between a genomic region and T1D risk. Instead, the work should narrow down to specific variant(s) and gene(s), and then use functional studies to show how those changes alter gene regulation or gene function in ways that contribute to T1D development.
What types of questions were projects expected to answer?
Projects were framed around identifying which specific DNA variants drive T1D risk, through what genes, in which cells, and by what regulatory or molecular mechanisms. The intent was to clarify disease pathogenesis, including immune dysregulation and beta cell biology influenced by inherited variation.
Were applicants encouraged to study loci without obvious candidate genes?
Yes. A key emphasis was that many T1D-associated loci do not clearly implicate one gene. Applicants were encouraged to do additional mapping and mechanistic studies to identify the causal gene(s) and causal variant(s) and then explain how altered gene function or regulation contributes to T1D.
What is the funding instrument type for this opportunity?
This was a discretionary grant program using the grant funding instrument type.
How was the activity area categorized?
The activity was categorized under Food and Nutrition/Health.
Which CFDA numbers were associated with this FOA?
The opportunity referenced multiple CFDA numbers, including 93.847 (Diabetes, Digestive, and Kidney Diseases Extramural Research) as well as 93.855 and 93.856 (allergy/infectious diseases and microbiology/infectious diseases). This reflects the immunologic and inflammatory dimensions of T1D research.
Was cost sharing or matching required?
No. Cost sharing or matching was not required.
How much total funding was estimated for the program?
The FOA listed an estimated total funding amount of $15,000,000.
What was the maximum award amount (award ceiling)?
The award ceiling was listed as $600,000.
Did the FOA specify how many awards would be made?
The information provided does not specify the number of awards. However, the presence of an estimated total program amount and a per-award cap suggests that multiple projects could be supported.
When was the opportunity posted?
The posting date and creation date were July 7, 2015.
What were the closing date and archive date?
The original and current closing date were February 17, 2016, and the archive date was March 19, 2016.
Is this funding opportunity still open?
No. Based on the listed closing and archive dates, the competition is closed. It remains relevant mainly as a historical reference for the types of studies NIH prioritized in this area at that time.
Who was eligible to apply?
Eligibility was broad and included public and private institutions of higher education; nonprofit organizations (with and without 501(c)(3) status); for-profit organizations (including small businesses and other for-profits); and many government entities, such as city or township governments, county governments, state governments, special district governments, independent school districts, and public housing authorities/Indian housing authorities.
Were community-focused and mission-specific institutions included in eligibility?
Yes. The eligibility language included HBCUs, Hispanic-serving institutions, tribally controlled colleges and universities, Alaska Native and Native Hawaiian serving institutions, AANAPISIs, faith-based or community-based organizations, U.S. territories or possessions, and regional organizations.
Were non-U.S. (foreign) organizations eligible?
Yes. The eligibility list included non-U.S. entities (foreign organizations).
What kinds of scientific teams did the FOA appear to be trying to attract?
The broad eligibility suggests an intent to attract a diverse range of scientific teams and institutional settings capable of conducting human genetics and functional genomics research relevant to T1D, including teams able to connect genetic variation to immune and pancreatic (beta cell) biology.
What was the intended impact or payoff of the supported research?
The intended payoff was to pinpoint causal biology rather than simply confirm association signals. The FOA aimed to produce insights that clarify T1D pathogenesis and could potentially inform new preventive or therapeutic directions by explaining how inherited variation influences immune pathways and beta cell biology.
Where could applicants or readers find the official FOA details?
The FOA pointed to the official NIH guide page at http://grants.nih.gov/grants/guide/rfa-files/RFA-DK-15-025.html.
Who was listed as a contact for access or linking issues?
The information provided indicates the NIH Office of Extramural Research webmaster contacts were provided for access or linking issues.
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