As wementioned that AK001796 could upregulate GAB1 expression through interactingwith miR-150 and competing with GAB1, we speculated that AK001796 could activateERK and Akt pathways through GAB1 to promote cell proliferation in HCC.Silencing the expression of AK001796 in HepG2 and SMMC-7721 cells, we found thatphospho-ERK1/2 and phospho-AKT were both decreased (Figure 7A). This evidence concerns the gene AKT1 and hepatocellular carcinoma.