VDAC1 and metabolic dysfunction-associated steatotic liver disease: In addition, after Cd exposure, VDAC1 formed dimers in the absence of VDAC1 upregulation, which was different from other findings that the dimerization of VDAC1 usually depended on its own upregulation in many pathological states such as NAFLD, cancer, Alzheimer's disease, and cardiovascular diseases.[27, 28] Further, dimerization of VDAC1 promoted its ubiquitination based on the fact that a specific inhibitor of VDAC1 oligomerization VBIT4 successfully inhibited VDAC1 ubiquitination in Cd's hepatotoxicity.[18]