ALKBH5 and metabolic dysfunction-associated steatotic liver disease: And ALKBH5-dependent demethylation drives lipogenesis and NAFLD-HCC progression via stabilizing LINC01468, which accelerates cullin4A (CUL4A)-linked degradation of inositol polyphosphate phosphatase-like 1 (INPPL1, SHIP2).308 Nevertheless, another study demonstrated that overexpressed ALKBH5 could ameliorate liver fibrosis and inactivate Hepatic stellate cells (HSCs) via upregulating Patched 1 (PTCH1).309 Moreover, YTHDF3 was also reported to restrain liver fibrosis and HSC activation via facilitating peroxiredoxin 3 (PRDX3) translation in an m6A-dependent manner.310