TP53 and neoplasm: Using ferroptosis as an example, the mouse p53 mutant with substitutions at K117, K161, and K162 (hereafter referred to as p53 3KR/3KR) can activate ferroptosis and suppress tumor growth; however, adding a fourth mutation at K98 abolishes the promotion of ferroptosis; further adding a fifth mutation at K136 completely diminishes the remaining tumor-suppressive function of p53.