TRPC4AP and type 2 diabetes mellitus: Interestingly, these polymorphisms were found to correlate with the tissue-specific expression of genes involved in the UPR pathway (EIF2S2, EIF6, UQCC1, PIGU, ITCH, TRPC4AP, EDEM2, TP53INP2, and MAP1LC3A), glucose-stimulated insulin secretion, and glucose uptake by cells (MYH7B, CPNE1, TRPC4AP, and NCOA6) [16], providing additional evidence for the existence of shared molecular mechanisms involved in the regulation of glutathione metabolism and protein folding, and linking them to the pathogenesis of type 2 diabetes.