A number of these groups were characterized by molecular processes well-known to be dysregulated in diabetic islets—such as potassium channels, glucokinase, incretin signaling, and Wnt signaling—while others were enriched for processes less established in the islet pathogenesis of T2D, such as insulin-, interleukin-, and ephrin-signaling, cell and adherens junctions and neurotransmitter release. This evidence concerns the gene KCNA3 and type 2 diabetes mellitus.