Therefore, aiming for GCH1/BH4 metabolism could increase erastin‐induced ferroptosis and thus limit CRC progression by activating iron phagosomes.[116] TP53‐induced glycolysis and apoptosis regulator (TIGAR) expression was remarkably increased in CRC tissues, and its inhibition downregulated the GSH/glutathione disulfide (GSSG) ratio, increased lipid peroxidation, enhanced MDA accumulation, and promoted erastin‐induced ferroptosis. The gene discussed is GCH1; the disease is colorectal carcinoma.