Importantly, we demonstrated that PKA/Runx2/Itgav signaling is a probable mechanism for regulating HSC activation in liver fibrosis, and pharmacological blockade of Itgav attenuated Runx2‐induced HSC activation and liver fibrosis, which suggests a critical and yet unappreciated role of Runx2 in the development and progression of liver fibrosis, and may provide a potential new therapeutic target for liver fibrosis. The gene discussed is ITGAV; the disease is Hepatic fibrosis.