In arteriovenous malformation caused by hereditary hemorrhagic telangiectasia, shear stress stimulates type I/II serine/threonine kinase receptor (ALKs) on the endothelial cell surface and regulates interaction between the receptor and bone morphogenetic proteins 9 and 10 (BMP9 and BMP10). This evidence concerns the gene BMPR1B and hereditary hemorrhagic telangiectasia.