In addition to AKT3, we in this present study also found that mTOR and its downstream target molecules p70S6K and eIF4EBP1 were all phosphorylated and activated by LINC00680 overexpression, whereas knockdown LINC00680 significantly inhibited their phosphorylation, suggesting that mTOR mediated p70S6K and eIF4EBP1 activation might play an integral role for transduction of LINC00680/miR-568/AKT3 signaling and the corresponding modulation of tumor stemness and chemosensitivity in HCC. This evidence concerns the gene AKT3 and neoplasm.