In contrast, Sun et al. showed that the inhibition of hepatocyte autophagy, in a manner dependent on mTOR, contributed to the alleviation of MASLD to fibrosis through the upregulation resulting from the knockdown of tet methylcytosine dioxygenase 3 (TET3), which reduced ectonucleotide phosphodiesterase 1 (ENPP1) expression in HFD-induced MASLD mice model [22]. The gene discussed is TET3; the disease is metabolic dysfunction-associated steatotic liver disease.