TP53 and pancreatic neoplasm: Recent findings showing that MDM2 controls glycolysis independently of p53 upon energetic shortage resulting from ETC-CI deficiency in conditions of high αKG levels, together with observations indicating that restoring WT-p53 functions in pancreatic cancer cells results in accumulation of αKG, suggest that this key metabolite is central to p53-associated metabolic networks [16,97].