The study investigates the role of activin receptor-like kinase 1 (ALK1) in vascular development and angiogenesis. ALK1, a type I receptor for transforming growth factor-β (TGF-β), is expressed in blood vessels and mutations in the *ALK1* gene are associated with hereditary hemorrhagic telangiectasia. To understand ALK1's function, researchers created ALK1-deficient mice by gene targeting. Homozygous ALK1 embryos died at mid-gestation, showing severe vascular abnormalities characterized by excessive fusion of capillary plexes and hyperdilation of large vessels. These defects are linked to enhanced expression of angiogenic factors and proteases, and impaired differentiation and recruitment of vascular smooth muscle cells. The vascular defects in ALK1-deficient mice are similar to those observed in mice lacking TGF-β1, TGF-β type II receptor (TβR-II), or endoglin, suggesting that ALK1 mediates TGF-β1 signaling in endothelial cells. The study demonstrates that ALK1 binds to TGF-β1 and TβR-II, and its signaling pathway can inhibit TGF-β1-dependent transcriptional activation mediated by ALK5. The results suggest that the balance between ALK1 and ALK5 signaling pathways in endothelial cells is crucial for determining vascular endothelial properties during angiogenesis.The study investigates the role of activin receptor-like kinase 1 (ALK1) in vascular development and angiogenesis. ALK1, a type I receptor for transforming growth factor-β (TGF-β), is expressed in blood vessels and mutations in the *ALK1* gene are associated with hereditary hemorrhagic telangiectasia. To understand ALK1's function, researchers created ALK1-deficient mice by gene targeting. Homozygous ALK1 embryos died at mid-gestation, showing severe vascular abnormalities characterized by excessive fusion of capillary plexes and hyperdilation of large vessels. These defects are linked to enhanced expression of angiogenic factors and proteases, and impaired differentiation and recruitment of vascular smooth muscle cells. The vascular defects in ALK1-deficient mice are similar to those observed in mice lacking TGF-β1, TGF-β type II receptor (TβR-II), or endoglin, suggesting that ALK1 mediates TGF-β1 signaling in endothelial cells. The study demonstrates that ALK1 binds to TGF-β1 and TβR-II, and its signaling pathway can inhibit TGF-β1-dependent transcriptional activation mediated by ALK5. The results suggest that the balance between ALK1 and ALK5 signaling pathways in endothelial cells is crucial for determining vascular endothelial properties during angiogenesis.