Hence, whereas further preclinical and clinical studies are necessary, our study suggests a potential antitumor therapeutic strategy based on targeting the p52-ZER6/G6PD/PPP axis both in patients with wild-type p53 and in those with mutant p53. This is of particular clinical importance as more than 50% of tumor patients harbor mutations in the p53 gene and wild-type p53 expression is aberrantly low, suggesting abnormalities in the p53 regulatory mechanism [39, 40]. The gene discussed is G6PD; the disease is neoplasm.