In solid cancers, microenvironment-derived CXCL12 has been shown to stimulate survival, growth, and migration of CXCR4-expressing cancer cells in a paracrine fashion [8, 9], to recruit (in an endocrine mechanism) endothelial progenitor cells to promote tumor vasculogenesis [10], and to direct circulating cancer cells to niches of high-level CXCL12 expression [5]. This evidence concerns the gene CXCR4 and neoplasm.