Instead, a 12-LOX-mediated, ACSL4-independent ferroptosis pathway plays an essential role in p53-dependent tumor suppression.31 In this pathway, p53 indirectly activates the function of 12-LOX through transcriptional inhibition of SLC7A11, leading to 12-LOX-dependent ferroptosis upon ROS stress.31 These findings delineate that both ACSL4/LPCAT3/15-LOX and p53/SLC7A11/12-LOX pathways contribute to lethal LPO production during ferroptosis. The gene discussed is TP53; the disease is neoplasm.