Having confirmed the ability of CFL1 to regulate sorafenib sensitivity, we further evaluated whether CFL1 could also regulate the sensitivity of HCC cells to other clinically used TKIs as the benefits of these TKIs for advanced HCC patients are very limited.[8] To this end, we down‐regulated CFL1 expression in MHCC‐97L cells and then, respectively, treated the cells with two clinically used TKIs, i.e., regorafenib and lenvatinib. This evidence concerns the gene CFL1 and hepatocellular carcinoma.