In addition, this pro-oxidant activity allows us to sensitize cancer cells to oxidative stress by blocking their antioxidant defense, resulting in cell death through inhibition of Nrf2 pathways and, in turn, of its downstream effectors, such as antioxidant enzymes (SOD, catalase) and glutathione (GSH), thioredoxin, and HO-1 systems [15]. This evidence concerns the gene HMOX1 and cancer.