We further demonstrated that the PlGF, which was induced by hypoxia during liver fibrosis dependent on HIF‐1α, was involved in HSC activation and proliferation through modulation of the PI3K/Akt signalling pathway (Fig. 8), while the addition of PI3K inhibitor to PlGF‐treated HSCs abrogated the proliferative and activated effects of PlGF. This evidence concerns the gene PGF and Hepatic fibrosis.