Though many studies showed the beneficial effect of HO-1 in tumor growth, recent studies also suggest an opposite function of HO-1 in cancer cells, where cancer cells could be killed by the application of HO-1 or its product CO, probably via multiple mechanisms, including the induction of ferroptosis, induction of metabolic exhaustion, and apoptosis of the cancer cells [23,24]. This evidence concerns the gene HMOX1 and neoplasm.