Since expression of CCN2 and integrins is enhanced during HSC activation and liver fibrosis [53-57], persistence of the activated fibrogenic phenotype in HSC may occur, at least in part, by NF-κB survival pathways that are triggered via the binding of CCN2 to its integrin αvβ3 receptor. The gene discussed is NFKB1; the disease is Hepatic fibrosis.