Since Sema7A is involved in atherosclerosis33, pulmonary fibrosis16, liver fibrosis50, and multiple sclerosis pathogenesis18 that are associated with EndMT5,8,35,51,52, our findings from both Sema7A-overexpressed cells and Sema7A-deficient mice provide a clue that Sema7A-β1 integrin and downstream signaling molecules could be regarded as promising targets for treatment of diseases associated with EndMT. The gene discussed is SEMA7A; the disease is multiple sclerosis.