Blocking SCD1/FADS2 contributed to increased cellular reactive oxygen species (ROS) and lipid peroxidation through downregulated glutathione peroxidase 4 (GPX4) and the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio in ascites-derived ovarian cancer cells, thereby promoting ferroptosis [62]. This evidence concerns the gene SCD and ovarian carcinoma.