The expression of molecular chaperones and genes involved in the UPR pathway in T2D patients was influenced by the expression of genes responsible for de novo biosynthesis of glutathione, GCLC, GCLM, and GSS, which supports the hypothesis that dysregulation of glutathione biosynthesis might be a key condition responsible for the impaired folding of proinsulin, triggering an unfolded protein response, and ultimately leading to β-cell apoptosis and type 2 diabetes [16]. This evidence concerns the gene GCLC and type 2 diabetes mellitus.