In two recent studies published in Nature, Wu et al. and Palma et al. elegantly demonstrated that the endogenous ferroptosis suppressor AIF family member 2 (AIFM2, best known as FSP1) is a pharmacologically actionable vulnerability in lung carcinoma and metastatic melanoma.1,2 These findings formally validate the notion that activating ferroptosis might constitute a viable strategy to control developing tumors (which often exhibit defects in apoptotic signaling),3 potentially paving the way to the development of clinically viable ferroptosis inducers for cancer therapy. This evidence concerns the gene AIFM2 and cancer.