It is worth noting that the withdrawal of the ferroptosis inhibitor ferrostatin-1 reduced tumor growth in the FSP1/GPX4 double knockout but not the GPX4 single knockout in the H460 lung cancer mouse xenograft model, indicating that targeting FSP1 may be a promising therapeutic strategy to overcome resistance to ferroptotic cell death in these clinical contexts [25]. This evidence concerns the gene GPX4 and lung carcinoma.