The binding of CD36 to ACSL1 acts as a “bridge” between long-chain fatty acids (LCFAs) and mitochondria, facilitating the transport of LCFA to ACSL1 and thereby enhancing fatty acid oxidation (FAO) in hepatocytes and mitigating lipid accumulation in NAFLD [74]. This evidence concerns the gene ACSL1 and metabolic dysfunction-associated steatotic liver disease.