As CCA was often initiated by biliary inflammation and cholestasis and it can be categorized into “inflammation” and “proliferation” based on the transcriptomic profile, NAFLD may elevate the risk of CCA by causing the inflammation response via the IL6-STAT3 signaling pathway and promoting cell growth via the receptor tyrosine kinase (RTK) signaling pathway (Wieckowska et al., 2008; Michelotti et al., 2013; Banales et al., 2020). This evidence concerns the gene STAT3 and metabolic dysfunction-associated steatotic liver disease.