However, the phosphorylation of AKT (Ser473 and Thr308), eNOS (Ser1177) and β-catenin in HUVECs was markedly increased after coculture with ANGPT2-overexpressing exosomes, and compared with control exosomes, the ANGPT2-deficient exosomes abrogated exosome-induced phosphorylation of these factors (Additional file 10: Figure S7), indicating that HCC cell-secreted exosomal ANGPT2 activated the AKT/eNOS and AKT/β-catenin pathways in HUVECs. Here, AKT1 is linked to hepatocellular carcinoma.