Correspondingly, researchers suggested that selective inhibition of CLCF1/CNTFR (ciliary neurotrophic factor receptor) or ERK1/2 in mouse models precluded crosstalk between CAFs and HCC cells, which might become a potential treatment for HCC patients since up-regulation of CLCF1-CXCL6/ TGF-β cascade in HCC patient samples was pertaining to poor prognosis [443]. This evidence concerns the gene MAPK3 and hepatocellular carcinoma.