Furthermore, HSC‐specific knockdown of Robo2 was achieved in a mouse model of liver fibrosis by using a recombinant adeno‐associated virus (AAV) vector to confirm the role of the receptor, and we proved that Robo2 knockdown inhibited the activation of HSC and liver fibrosis, which also led to the inactivation of Smad2/3 and PI3K/Akt pathways in sTREM‐1‐induced HSC activation and liver fibrosis. The gene discussed is AKT1; the disease is Hepatic fibrosis.