In type 1 diabetes (T1D), insulin secretion is rapidly lost due to autoimmune-selective β-cell destruction (Siafarikas et al., 2012), whereas in type 2 diabetes (T2D), the delayed onset and gradual progression of insulin deficiency reflect exhausted β-cell efforts to compensate for insulin resistance (Weir et al., 2001). This evidence concerns the gene INS and type 2 diabetes mellitus.