Since T2D-associated alleles of genes for glutathione metabolism (e.g., GSS and GGT7) correlate with expression levels of genes involved in the unfolded protein response pathway and regulation of proteostasis [240], it can be hypothesized that glutathione deficiency in beta-cells of pancreatic islets may contribute to the impaired folding of proinsulin identified in type 2 diabetes. The gene discussed is GGT7; the disease is type 2 diabetes mellitus.