At the tumor site, the released Fe3+ and Fe2+ may catalyze the reactions to produce LPOs, resulting in ferroptosis, specifically in the H2O2‐overloaded cancer cells.[24] Meanwhile, RSL3 lead to GPX4 inhibition, which then leads to ferroptosis induction in cancer cells.[25] In general, this study reveals a new therapeutic strategy using a PSMA‐specific, CRPC‐targeting platform of ferroptosis induction with increased efficacy and safety; our results may also expand the current of ferroptosis in the CRPC landscape. This evidence concerns the gene FOLH1 and cancer.