Further, it was recently reported that KRAS, which was found mutation/amplification in nearly 13.9% of ovarian cancers [29], may play a role in ferroptosis and lipid biosynthesis [30], while other studies found that mutant KRAS activates the NRF2 antioxidant pathway, in which NRF2 activated glutaminolysis and glutamine deprivation resulted in reduced GPX4 levels [31]. The gene discussed is GPX4; the disease is ovarian carcinoma.