AKT1 and neoplasm: We previously established hypoxic HSC-derived PDGF-ββ stimulates the proliferation of HCC cells by activating the PI3K/Akt pathway, while the inhibition of PDGF-ββ or PI3K/Akt pathway enhances apoptotic cell death, indicating targeting tumor-stroma crosstalk might be a novel therapy for the management of human HCC [14].