Endothelial deletion of α-parvin perturbs both cell–matrix and cell–cell adhesions, leading to angiogenesis and barrier defects in mice, which is at least partially due to differences in Rac and Rho activities.68 A similar phenotype is seen in endothelial ILK knockout mice, while in humans, mutations in ILK have been disclosed in familial exudative vitreoretinopathy.69 The gene discussed is ILK; the disease is exudative vitreoretinopathy.