Therefore, a decrease in the intracellular α-KG levels due to overexpression of the α subunit of isocitrate dehydrogenase 3 (IDH3), IDH3α [37], or mutations and resultant amino acid substitutions in succinate dehydrogenase (SDH) or fumarate hydratase (FH) in the TCA cycle of cancer cells results in the activation of HIF-1 by keeping P402, P564, and N803 unhydroxylated, even under normoxic conditions [35,36,37]. This evidence concerns the gene HIF1A and cancer.