Two crucial discoveries motivated the research on SAM’s therapeutic role against liver preneoplastic and neoplastic lesions: the Mat1A/Mat2A switch with consequent decrease in SAM synthesis in HCC [15] and the decrease of SAM, associated with steatosis, in liver of ethanol-intoxicated rats [20] and in preneoplastic and neoplastic rat liver [17]. The gene discussed is MAT1A; the disease is steatosis.