In HCC, EMT is characterized by vimentin-expressing cells, as observed in metastatic lymph nodes, and by immunosuppressive changes in the tumor microenvironment.16,17) Phenotypic changes in tumor cells associated with EMT can alter the expression of immune checkpoint molecules such as PD-L1 and CTLA-4, thereby promoting resistance to immunotherapy.18) The mesenchymal marker expression pattern in our case was consistent with EMT, suggesting resistance to Dur and Tre compared with conventional HCC.19). This evidence concerns the gene CTLA4 and hepatocellular carcinoma.