Further evidence to corroborate hemangioblasts come from the expression of various genes such as CD34 and Tie2 by both lineages. The fact that this expression was seen in both EC and HPC lineages led researchers to propose a common origin. However, endothelial markers like Flk1/VEGFR-2 are exclusive to ECs but stop HPCs from progressing into an EC. It is accepted that VEGFR-2+ cells are a common precursor for HPCs and ECs. If the "Vegfr3" gene is deleted then both HPC and EC differentiation comes to a halt in embryos. VEGF promotes angioblast differentiation; whereas, VEGFR-1 stops the hemangioblast from becoming an EC. In addition, basic fibroblast growth factor FGF-2 is also involved in promoting angioblasts from the mesoderm. After angioblasts commit to becoming an EC, the angioblasts gather and rearrange to assemble in a tube similar to a capillary. Angioblasts can travel during the formation of the circulatory system to configure the branches to allow for directional blood flow. Pericytes and smooth muscle cells encircle ECs when they are differentiating into arterial or venous arrangements. Surrounding the ECs creates a brace to help stabilize the vessels known as the pericellular basal lamina. It is suggested pericytes and smooth muscle cells come from neural crest cells and the surrounding mesenchyme.