In vitro studies that explored the pathogenesis of arsenic-induced T2DM have implicated the involvement of several biological processes, including the protein kinase B (PKB/Akt) pathway [19], [20], calcium-dependent calpain-10 proteolysis of SNAP-25 [21], [22], cellular adaptive response of oxidative stress [23], [24], inhibition of glucose-dependent insulin secretion [25],and endoplasmic reticulum stress [26]. The gene discussed is AKT1; the disease is type 2 diabetes mellitus.