Considerable clinical research evidence indicates that inactivation of tumor suppressor genes (TP53, BRCA1, and PTEN) or activation of oncogenes (Myc, Ras, and EGFR) leads to a robust increase in the metabolic demands of cancer cells 32, resulting in a rapid increase in protein synthesis and then inducing ER stress or activation of an adaptive UPR pathway, which promotes cancer progression. Here, TP53 is linked to cancer.