On the other hand, it was reported that Gnmt mRNA levels were suppressed in patients with advanced nonalcoholic fatty liver disease (NAFLD) [36] and Gnmt deficiency and/or hypermethioninemia, and elevated SAM levels could play a role in the pathogenesis of NAFLD by inhibiting lipophagy through PP2A methylation in an mTORC1-independent mechanism [37]. This evidence concerns the gene PTPA and metabolic dysfunction-associated steatotic liver disease.