A recent study by Yamamoto et al., showed HO-1 vicarious contribution, through its end-product CO, to cancer cells adaptation to oxidative stress condition and drugs through the inhibition of heme-containing cystathionine β-synthase, resulting in decreased methylation of PFKFB3, an enzyme producing fructose 2,6-bisphosphate (F-2,6-BP), and shift of glucose metabolism to the pentose phosphate pathway (PPP), causing a subsequent increase in NADPH to restore reduced GSH pool [183]. The gene discussed is HMOX1; the disease is cancer.