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 This evidence concerns the gene ILK and Familial exudative vitreoretinopathy.