Murphy and colleagues showed that a polymorphic variant of p53 was able to induce growth arrest and senescence in both human and murine cells but failed to repress SLC7A11 or transactivate GLS2. This variant was markedly impaired at inducing ferroptosis and suppressing tumor development, thus again implicating the role of p53 in ferroptosis-mediated tumor suppression (48). The gene discussed is GLS2; the disease is neoplasm.