This enhanced ability of the CAFs to stimulate the previously described CSC growth/pro-angiogenic program [5], especially in response to an early stage tumor microenvironment (e.g., growth on Matrigel), is in line with in vivo experiments in which (a) subcutaneous tumors originating from CSCs gave rise to a more abundant vascular network composed of larger vessels than the tumors originating from CPCs, (b) the tumors of the CSC-injected mice had increased Ki-67 staining for mitotic index [5] and (c) grow faster than those in mice injected with CPCs [29]. Here, MKI67 is linked to neoplasm.