Abnormally high cholesterol in hepatocellular carcinoma cells promotes malignant lesions in non-alcoholic fatty liver disease (NAFLD) by inducing lncRNA SNHG6 to localize in the endoplasmic reticulum-lysosome interactions region and activating the mammalian target of rapamycin (mTORC1) signaling pathway [115]. Here, MTOR is linked to metabolic dysfunction-associated steatotic liver disease.