Whereas mechanistically, functional disorders of tumor suppressors or oncogenes lead to unbalance of ferroptosis promotion systems (polyunsaturated fatty/PUFA synthesis and peroxidation, iron metabolism, and mitochondrial metabolism) and/or ferroptosis defense systems (GPX4‐GSH system, FSP1‐CoQH2 system, and DHODH‐CoQH2 system), which renders cancer cells vulnerable or resistant to ferroptosis.[5, 6]. This evidence concerns the gene DHODH and cancer.