The weakened activity of ALKBH5 reduced the stability of AXL mRNA in hepatocytes and downregulated AXL expression, which further suppressed the MAPK/ERK signaling pathway, thus enhancing liver autophagy flux and reducing liver lipid deposition and, finally, improving HFD-induced MASLD [76]. This evidence concerns the gene ALKBH5 and metabolic dysfunction-associated steatotic liver disease.