According to a recent study, prolargin was solely expressed and secreted by a subset of CAFs deriving from portal fibroblasts, which bound and antagonized several pro-angiogenic growth factors, such as FGF1, FGF2, HGF, and TGF-β1, to inhibit the angiogenesis of HCC and was positively correlated with good clinical outcome in HCC patients [45]. The gene discussed is FGF2; the disease is hepatocellular carcinoma.