The inhibition of heat shock protein 90 beta (HSP90β) facilitates the ubiquitination and proteasomal degradation of mature sterol regulatory element-binding proteins (SREBPs), leading to the amelioration of lipid metabolism disorders in patients with nonalcoholic fatty liver disease (NAFLD) and diet-induced obese (DIO) mice [20]. This evidence concerns the gene HSP90AB1 and metabolic dysfunction-associated steatotic liver disease.