RPL23A and metabolic dysfunction-associated steatotic liver disease: In contrast to normal liver cells that progress to NAFLD&NASH, RPL23A regulated by hypomethylation caused defects in the autoimmune response to promote more severe liver damage through the WNT and the MAPK signaling pathways, and HIST2H2BE was also regulated by hypermethylation to facilitate abnormal DNA repair through the MAPK signaling pathway in the progression of normal liver cells to PBC&PSC, as shown in Figure 3.