MTOR and cancer: For example, in human cancers, a consequence of gain-of-function mutations in isocitrate dehydrogenases (IDHs) confers to the enzyme the ability to augment the production of D-2-hydroxyglutarate (D-2HG), an oncometabolite interfering with various α-KG (α-ketoglutarate)-mediated processes, ultimately leading to the inhibition of mitochondrial ATP synthase and activation of a series of downstream signals that involve mammalian target of rapamycin (mTOR) suppression [13,14].