Upon Complex I inhibition, NADH accumulation allosterically inhibits the TCA cycle enzyme α-ketoglutarate (αKG) dehydrogenase, thereby increasing the α-ketoglutarate/succinate (αKG/Suc) ratio, which favors the activity of the prolyl-hydroxylases in charge of the degradation of HIF1α, and causing tumor growth arrest (18, 34, 35). This evidence concerns the gene HIF1A and neoplasm.