Such cancer hallmark capabilities reflect, at least, in part some acquired aberrations in mitochondrial function- preferably a shift from OXPHOS to glycolysis (41); the latter is achieved through inhibition of pyruvate dehydrogenase complex (PDH) by PDK1 thus inhibiting/abrogating the entry of Acetyl CoA (ac CoA) to fuel tricarboxylic acid (TCA) cycle and OXPHOS (42, 43). This evidence concerns the gene PDK1 and cancer.