This conclusion is supported by the facts that VEGFR-2+/CD133+ GSLCs are capable of differentiating into EC and EC-like cells; that some CD133+ GSLCs constitutively express both VEGFR-2 and VEGF, which promote their differentiation into EC-like cells in an autocrine or paracrine manner; that blood vessels and VM in xenograft tumors initiated by VEGFR-2+/CD133+ GSLCs are mainly derived from transplanted human tumor cells; and that the vasculature in xenograft tumors formed by GSLCs containing VEGFR-2 shRNA was formed mostly by mouse-derived ECs. The gene discussed is KDR; the disease is neoplasm.