Prohibitin 2 (PHB2), a mitochondrial inner membrane protein essential for the maintenance of mitochondrial structure and function, has been found its deletion in hepatocytes leads to mitochondrial fragmentation, disrupted lipid and glucose metabolisms, and increased liver triglyceride accumulation, which impairs mitophagy, disrupts mitochondrial function, and aggravates liver steatosis and inflammation, and is closely associated with the occurrence and development of NAFLD (76). This evidence concerns the gene PHB2 and metabolic dysfunction-associated steatotic liver disease.