Moreover, mouse phenotypes resulting from targeted disruption of TGF-βRII, endoglin or activin receptor-like kinase 1(ALK1) are highly reminiscent of TGF-β1 null mice, showing vascular abnormalities characterized by systemic vascular dysplasia and recurrent hemorrhage caused by telangiectases and arteriovenous malformations [100]. This evidence concerns the gene ACVRL1 and Telangiectasia.