Yoshida et al. observed that the NOX subunit p22phox is expressed in preneoplastic hepatic foci during HFD-induced hepatocarcinogenesis, and the mineralocorticoid spironolactone in combination with β-glycosyl isoquercitrin is able to prevent these steatosis-induced precancerous lesions by reducing p67phox expression and the number of p22phox-positive cells [73]. The gene discussed is CYBA; the disease is steatosis.