Treatment of non-diabetic mouse islets with oligomycin [10] and dinitrophenol [14], which inhibit mitochondrial ATP synthase and thus increase the KATP-channel conductance, cause typical T2DM ‘right-shift’ in glucagon secretion, i.e. inadequate secretion at low glucose and unsuppressed secretion at high glucose. The gene discussed is GCG; the disease is type 2 diabetes mellitus.