It has been reported that Hrd1 can ubiquitinate ACLY, leading to its protein degradation in non-alcoholic fatty liver disease (NAFLD) [74], and that the TGFβ1-CUL3-KLHL25 axis mediates ACLY ubiquitination and degradation to regulate immune cell differentiation and increase immune homeostasis in the human body [75]. This evidence concerns the gene ACLY and metabolic dysfunction-associated steatotic liver disease.