To confirm that AKT phosphorylation mediated the lncRNA AGAP2-AS1/miR-16-5p/ANXA11 axis biological function, we first confirmed that ANXA11 overexpression significantly increased, while ANXA11 knockdown decreased the phosphorylated AKT in HCC cells (P < 0.05, respectively, Fig. 9a). The gene discussed is AKT1; the disease is hepatocellular carcinoma.