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For example, the regulation of GPX4 by SRSF9 serves as a crucial mechanism that drives colorectal cancer tumorigenesis, as well as Erastin-induced ferroptosis resistance (76), and TP53-induced glycolysis and apoptosis regulator (TIGAR) functions as a potential modulator of ferroptosis resistance in colorectal cancer through the ROS/AMPK/SCD1 signal pathway, with the knockdown of TIGAR causing elevated lipid peroxidation and sensitive to erastin-induced ferroptosis (77)

They might cause certain allergic reactions if not done properly. 2