Induction of such shared cellular phenotypes consequent to AURKA overexpression or functional inactivation of TP53 as well as reported localization of the two proteins at the centrosomes indicate that AURKA and TP53 (hereafter referred to as Aurora-A and p53) are involved in overlapping signaling pathways regulating the abovementioned cancer-associated aberrant cellular phenotypes through direct or indirect functional interactions (1–5). The gene discussed is TP53; the disease is cancer.