Our data suggest that increased expression of CADM2, and reduced expression of TRPM5, PDK4, and/or ANGPTL4 could play a role in the development of both human T1D and NOD disease by altering mechanisms that control insulin sensitivity, insulin secretion, β-cell and pancreas development, and/or islet cell organization. This evidence concerns the gene ANGPTL4 and type 1 diabetes mellitus.