The outcome of signaling by TGF-β family members in ECs is highly context dependent. The net effect of stimulation or inhibition of EC migration, proliferation, and survival is illustrated by images from immunostaining of tumor sections for the vascular marker CD31 (red; images are only representations and are not derived from actual experimental settings). (A) TGF-β signaling through ALK1 predominantly acts to stimulate EC growth and migration. TGF-β signaling through ALK5 predominantly acts to inhibit EC growth and migration. BMP9 stimulation of ALK1 has been reported to be either inhibitory or stimulatory in terms of EC growth and migration. Stimulation of ECs with both TGF-β and BMP9, thus engaging both ALK1 and ALK5 simultaneously, primes ECs to an angiogenic stimulus by prototypical angiogenic inducers such as VEGF. (B) Representation of paracrine interaction between ALK1 expressed by ECs and ALK5 expressed by mural cells. (C) Illustration of the large complexity of BMP ligands and type I receptors that collectively regulate EC functionality in a context-dependent manner.