Opportunity Information: Apply for RFA DK 11 019
Apply for RFA DK 11 019
- The National Institutes of Health in the food and nutrition health sector is offering a public funding opportunity titled "Function of Type 1 Diabetes Genes (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.
- This funding opportunity was created on Oct 3, 2011 and posted on Oct 3, 2011.
- Applicants must submit their applications by Feb 29, 2012. (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.
- Eligible applicants include: Native American tribal organizations (other than Federally recognized tribal governments) Others (see text field entitled Additional Information on Eligibility for clarification) Private institutions of higher education County governments City or township governments Nonprofits that do not have a 501(c)(3) status with the IRS, other than institutions of higher education Small businesses For profit organizations other than small businesses State governments Special district governments Public and State controlled institutions of higher education Native American tribal governments (Federally recognized) Independent school districts Public housing authorities/Indian housing authorities Nonprofits having a 501(c)(3) status with the IRS, other than institutions of higher education.
- Other Eligible Applicants include the following Alaska Native and Native Hawaiian Serving Institutions 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) Regional Organizations Tribally Controlled Colleges and Universities (TCCUs) U.S. Territory or Possession Non domestic (non U.S.) Entities (Foreign Institutions) are eligible to apply. Non domestic (non U.S.) components of U.S. Organizations are eligible to apply. Foreign components, as defined in the NIH Grants Policy Statement, are allowed.
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Opportunity Summary:
The Function of Type 1 Diabetes Genes (DP3) funding opportunity (RFA-DK-11-019) was a discretionary NIH grant program run by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) to push the field beyond genetic association signals and toward concrete biological explanations of type 1 diabetes (T1D) risk. The FOA specifically invited DP3 Research Project Grant applications aimed at figuring out what T1D-associated genes actually do, with a strong emphasis on both human leukocyte antigen (HLA) genes and non-HLA genes implicated by human genetics. The central idea was to support ambitious, function-focused studies that can connect genetic variation to changes in gene regulation or protein function, then link those changes to immune biology, beta cell biology, and ultimately disease mechanisms.
A major motivation highlighted in the announcement is that, while many T1D risk regions have been mapped in humans, a large number of those regions still lack a clear functional “winner†gene or definitive causal variant. NIDDK therefore encouraged projects that (1) identify the most likely causal genes within known T1D loci, (2) pinpoint potential causal variants (for example, variants that alter regulatory elements, gene expression, splicing, or protein structure), and (3) explain the mechanism by which altered gene function or regulation contributes to T1D pathogenesis. In practice, this means proposals were expected to move from statistical association toward experimentally supported causality, ideally producing mechanistic insight that could guide new therapeutic or preventive strategies.
The opportunity was funded as a grant mechanism (DP3) under the broad health category, listed with CFDA number 93.847 (Diabetes, Digestive, and Kidney Diseases Extramural Research). The FOA projected an estimated total funding level of about $15,000,000. It did not require cost sharing or matching, which typically makes participation more feasible for a wide range of institutions and reduces barriers for investigators proposing resource-intensive functional genomics or mechanistic biology work.
Eligibility was intentionally broad. A wide range of domestic U.S. applicants could apply, including public and private institutions of higher education, nonprofits (including those with and without 501(c)(3) status, with the usual distinctions), small businesses, for-profit entities (including those other than small businesses), and many types of government entities (state, county, city/township, special districts, independent school districts, and public housing authorities/Indian housing authorities). The FOA also explicitly included numerous mission-focused or underserved-serving organizations such as Historically Black Colleges and Universities (HBCUs), Hispanic-serving institutions, Alaska Native and Native Hawaiian Serving Institutions, and Tribally Controlled Colleges and Universities (TCCUs), as well as federally recognized and other tribal organizations and governments. Importantly, non-U.S. entities (foreign institutions) were eligible to apply, non-U.S. components of U.S. organizations were eligible, and foreign components were allowed as defined by NIH policy, signaling an openness to international expertise and globally distributed resources relevant to T1D genetics and functional validation.
In terms of timing, the FOA was posted and created on October 3, 2011, with an original and final application closing date of February 29, 2012. The opportunity later moved to archive status on March 31, 2012, meaning it was no longer active for new submissions after that cycle. The official full announcement was made available through the NIH Grants Guide at the provided link, and NIH’s Office of Extramural Research web support contacts were listed for access or linking issues.
Overall, this DP3 announcement can be read as a targeted push to translate T1D genetic discoveries into experimentally grounded biology: clarifying which genes and variants matter, how they act in relevant cell types and pathways, and why those molecular effects increase the likelihood of autoimmunity and beta cell loss. The expected payoff was not simply another catalog of associations, but clearer causal stories that can reshape how researchers think about T1D development and how they design future interventions.
Frequently Asked Questions (FAQs)
What is this funding opportunity?
The Function of Type 1 Diabetes Genes (DP3) funding opportunity (RFA-DK-11-019) was a discretionary NIH grant program run by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). It supported DP3 Research Project Grants focused on understanding what type 1 diabetes (T1D)-associated genes actually do, moving beyond genetic association signals toward clear biological mechanisms.
What was the main goal of RFA-DK-11-019?
The main goal was to push the field from statistical genetic associations to experimentally supported, mechanistic explanations of T1D risk. Projects were expected to connect genetic variation to changes in gene regulation or protein function, and then link those changes to immune biology, beta cell biology, and disease mechanisms.
Which NIH institute ran this program?
The program was run by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH).
What grant mechanism was used?
The opportunity used the DP3 Research Project Grant mechanism.
What types of research did the FOA specifically invite?
The FOA invited ambitious, function-focused studies aimed at figuring out the biological roles of T1D-associated genes. It emphasized projects that could translate genetic discoveries into concrete functional and mechanistic insights relevant to T1D pathogenesis.
Did the FOA focus on specific categories of T1D genes?
Yes. The FOA emphasized both human leukocyte antigen (HLA) genes and non-HLA genes implicated by human genetics.
Why did NIDDK consider this program necessary?
A key motivation described in the announcement was that, although many T1D risk regions had been mapped in humans, many of those regions still lacked a clear functional "winner" gene or a definitive causal variant. The program was designed to help close that gap by supporting studies that could identify causal genes/variants and explain how they contribute to disease.
What kinds of deliverables or scientific advances was NIDDK looking for?
Based on the description, the program prioritized mechanistic insight over additional association catalogs. Expected advances included experimentally grounded causal stories: which genes and variants matter, how they act in relevant cell types and pathways, and why those molecular effects increase the likelihood of autoimmunity and beta cell loss.
What were the encouraged scientific aims for applicants?
NIDDK encouraged projects that: (1) identify the most likely causal genes within known T1D loci, (2) pinpoint potential causal variants (for example, variants altering regulatory elements, gene expression, splicing, or protein structure), and (3) explain the mechanism by which altered gene function or regulation contributes to T1D pathogenesis.
What is meant by moving from "association" to "causality" in this FOA?
In this context, it meant moving beyond statistical links between DNA regions and disease risk and instead producing experimental evidence that a specific gene and/or variant changes biological function (such as gene regulation or protein activity) in a way that plausibly drives T1D-related immune or beta cell processes.
Was this opportunity limited to U.S. institutions?
No. The FOA explicitly stated that non-U.S. entities (foreign institutions) were eligible to apply. It also allowed non-U.S. components of U.S. organizations and foreign components as defined by NIH policy.
Who was eligible to apply?
Eligibility was broad and included many domestic U.S. applicant types such as public and private institutions of higher education, nonprofits (including those with and without 501(c)(3) status), small businesses, for-profit entities (including those other than small businesses), and multiple levels and types of government entities (for example, state, county, city/township, special districts, independent school districts, and public housing authorities/Indian housing authorities). The FOA also explicitly included HBCUs, Hispanic-serving institutions, Alaska Native and Native Hawaiian Serving Institutions, Tribally Controlled Colleges and Universities (TCCUs), federally recognized tribes and other tribal organizations, and tribal governments.
Were for-profit organizations allowed to apply?
Yes. The eligibility description included for-profit entities, including those other than small businesses.
Were nonprofits without 501(c)(3) status eligible?
Yes. The eligibility list included nonprofits with and without 501(c)(3) status (with the usual distinctions referenced in the summary).
Could tribal organizations and tribal governments apply?
Yes. The FOA explicitly included federally recognized and other tribal organizations and governments, as well as Tribally Controlled Colleges and Universities (TCCUs).
Did the FOA require cost sharing or matching funds?
No. The FOA did not require cost sharing or matching.
How much funding was projected for this program?
The FOA projected an estimated total funding level of about $15,000,000.
What CFDA number was associated with this opportunity?
The program was listed with CFDA number 93.847 (Diabetes, Digestive, and Kidney Diseases Extramural Research).
When was the FOA posted and when were applications due?
The FOA was posted/created on October 3, 2011. The original and final application closing date was February 29, 2012.
Is this funding opportunity still open?
No. The opportunity moved to archive status on March 31, 2012, which indicates it was no longer active for new submissions after that cycle.
Where was the official announcement published?
The official full announcement was made available through the NIH Grants Guide at the link referenced in the opportunity description.
What kind of support contact was mentioned for technical issues?
NIH Office of Extramural Research web support contacts were listed for access or linking issues related to the announcement.
How does this FOA relate to therapy or prevention?
The FOA framed mechanistic understanding as a way to guide future therapeutic or preventive strategies. The intended payoff was clearer causal biology that could reshape how researchers think about T1D development and inform future intervention design.
What disease processes did the FOA want applicants to connect genetics to?
The FOA emphasized linking genetic variation and gene/protein function to immune biology, beta cell biology, and ultimately the mechanisms that lead to T1D pathogenesis (including autoimmunity and beta cell loss).
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