In the present study, we have shown that the combination of emodin and sorafenib functioned synergistically to increase cell cycle arrest and the proportion of apoptotic cells, which was consistent with the observed decrease in cell viability, through the suppression of oncogenic AKT signaling and activation of signal transducer and activator of transcription 3 (STAT3) in HCC cells. Here, AKT1 is linked to hepatocellular carcinoma.