In the MAT1A knockout (MAT1A-KO) mouse model, which shows a chronic deficiency in SAMe levels and, spontaneously, develops NASH and HCC, hepatic levels of LKB1 and AMPK are activated, incrementing the cytoplasmic localization of HuR, which leads to the stabilization and expression of cyclin A2 and D1 mRNAs, and subsequent cell cycle progression [195]. The gene discussed is MAT1A; the disease is metabolic dysfunction-associated steatohepatitis.