Thus beta-cell ncNOS is conveniently located to immediately impact and regulate the secretory machinery after acute glucose stimulation, while iNOS-derived NO has been shown to be insufficient in this context [17] and more likely contributes to β-cell dysfunction during persisting hyperglycemia and/or hyperlipidemia and the development of nonimmunogenic type 2 diabetes over time [8,9,15,18–23]. The gene discussed is NOS1; the disease is type 2 diabetes mellitus.