Given that no second‐line drugs are available after the failure of sorafenib (Chan et al., 2016), the results presented herein warrant clinical investigation of dual inhibition of c‐Met and Akt pathways, such as the combination of MK2206 and capmatinib, particularly as a second‐line therapy for advanced HCC that becomes acquired resistant to sorafenib. This evidence concerns the gene MET and hepatocellular carcinoma.