The theory that considers hyperlipidemia as a primary cause of B-cell dysfunction instead of hyperglycemia [26] (as it is reported that elevated free fatty acids and other lipids can impair B-cell function) is corroborated by the findings that GSTM1 does not influence the risk of T2DM but instead alters glycemic control along with GSTT1 polymorphism association with increased susceptibility to T2DM with only an alteration to lipid metabolism. The gene discussed is GSTM1; the disease is Hyperglycemia.