HIF1A and neoplasm: Recent in vitro and in vivo experiments suggest that an increase in the intracellular level of AKG through different strategies, e.g., exogenous supplementation, alpha-ketoglutarate dehydrogenase (KGD; an enzyme that catalyses the oxidative decarboxylation of AKG to succinyl-Co-A in the TCA cycle) inactivation or even IDH overexpression, may lead to downregulation of HIF-1 or upregulation of epigenetic enzymes and prevent/inhibit tumor progression or show direct anticancer effects [17,19,20,21,22,23,24].