Steatosis, fibrosis, and HCC develop spontaneously in mice deficient for glycine N-methyltransferase (Gnmt), which encodes an enzyme that catalyzes the transfer of a methyl group to glycine as a way to regulate cellular SAM levels and prevent aberrant methylation of other substrates (Martinez-Chantar et al. 2008). The gene discussed is GNMT; the disease is steatosis.