In established human liver fibrosis, regardless of aetiology (hepatitis B or C, autoimmune, alcohol‐induced or primary biliary cirrhosis), PlGF expression was undetectable in control normal liver and dramatically increased in the cirrhotic nodules of hepatocytes and non‐parenchymal cells, particularly at the portal tracts and fibrous septa, which was partly associated with neovessels in the hepatic scar as shown by immunohistochemistry (IHC) (Fig. 2A). Here, PGF is linked to Hepatic fibrosis.