19 showing that HGF induced EMT via the ERK pathway but not the Akt pathway in HCC cells. The activated PI3K/Akt pathway might promote sorafenib resistance via other mechanisms instead of EMT. It was reported that the PI3K/Akt pathway had a vital role in survival and proliferation, and its alteration in cancer cells exploits normal mechanisms to overcome apoptosis 31. Our previous reports showed that the activated PI3K/Akt pathway mediated acquired resistance to sorafenib in HCC by increasing the anti‐apoptotic protein Mcl‐1 and Bcl2 levels 12. This evidence concerns the gene AKT1 and hepatocellular carcinoma.