Given that ANIT is metabolized by hepatocytes and secreted into bile to damage cholangiocytes [31], our observation of TFNAs-induced ERK1/2 phosphorylation in the liver suggests that TFNAs may alleviate cholestasis by enhancing cholangiocyte repair via ERK1/2 activation (Figure 5). This evidence concerns the gene MAPK3 and cholestasis.