Studies have shown that SQLE is significantly upregulated in patients with NAFLD-related HCC; mouse hepatocyte-specific overexpression of SQLE drives cholesterol biosynthesis and the NADP/NADPH ratio, triggering an oxidative stress response that activates the DNA methyltransferase 3A-mediated PTEN/PI3K/AKT/mTOR signaling pathway, driving NAFLD-related HCC carcinogenesis; and the SQLE inhibitor terbinafine inhibits NAFLD-related HCC cell proliferation and tumor development in a mouse model (Liu et al., 2018). Here, MTOR is linked to metabolic dysfunction-associated steatotic liver disease.