TP53 and cancer: Since these signaling pathways are often hyper-activated in cancer due to oncogenes activation (e.g., K-RAS, MYC, and growth factor receptors), or oncosuppressors inactivation (e.g., p53 and PTEN loss-of-function and inactivation), any alterations that impact on these players may lead to G6PDH enhanced expression and activity (8, 9).