A major premise of DYNAMO has been that genomics holds great promise for defining primary features of DN pathophysiology and identifying potential therapeutic targets. Challenges with human GWAS studies in DN have included lack of diversity of study participants, GWAS signals often localizing to noncoding regions where the functional variant or gene is unknown, and limitations of reliance on susceptibility traits rather than variables reflecting disease progression. We will attempt to subvert these issues through: (1) multi-ancestry fine mapping in our diverse multi-ethnic cohorts, (2) integration of multi-omics data to prioritize variants at GWAS loci, and (3) focusing on the trait of progressive GFR decline, a key target for human therapeutics in DN.