In retrospect, the case-only interaction analyses based on MYH9 (and APOL1) risk variants likely segregated clinically diagnosed cases of T2DM-ESRD into those enriched for non-diabetic nephropathy (c22 nephropathy risk homozygotes with disease in the FSGS spectrum) and non-c22 homozygotes enriched for true DN. This evidence concerns the gene APOL1 and type 2 diabetes mellitus.