The roles of Gnas, Gprasp1, Krt7, and Gcp4 have been reported in glycolipid metabolism,[41, 42, 43, 44] among which Gnas plays a key role in regulating β cell function and has been listed as a candidate gene for T2D pathogenesis.[28, 29, 40]Krt7 is a constituent of the keratin network in mouse islets; however, Krt7 is not expressed in human pancreatic islets under basal conditions.[45] Gcp4 is located in the membrane,[44] indicating an indirect interaction and regulation between Tipe1 and Gcp4. This evidence concerns the gene GPRASP1 and type 2 diabetes mellitus.