In addition to the well-established regulation of LDLR activation by SREBFs and HNF4A, YY1 and KLF13, two specific TFs regulating the disease-associated modules, also showed a regulatory role in the transcriptional regulation of LDLR. Taken together, the complicated regulation of LDLR in the disease-associated modules rather than endocytosis in normal liver tissue might play an essential role in the dysregulation of lipid metabolism underlying the NAFLD pathogenesis. This evidence concerns the gene YY1 and metabolic dysfunction-associated steatotic liver disease.