CD18–/– mice show a cell-autonomous defect of migration of leucocytes to the site of inflammation.96,115 The similarity of the Hck–/–Fgr–/–Lyn–/–, Syk–/–, PLCγ2–/–, and Vav1–/–Vav2–/–Vav3–/– phenotypes to that of CD18–/– mice, together with the known role of Src-family kinases, Syk, PLCγ2, and Vav family members in integrin outside-in signal transduction96,99,106,125–127 suggested that the protection of all those mutants from leucocyte accumulation and arthritis development are due to a cell-autonomous defect of CD18-mediated leucocyte migration. Here, VAV1 is linked to arthritic joint disease.