Among potential mechanisms facilitating this environment are the physical exclusion of T cells from tumor nests through an aberrant vasculature, the engagement of different chemokine signaling pathways, including transforming growth factor-β (TGFβ) and CXCL12 (refs. 41–44), or an insufficient availability of tumor-specific/tumor-associated antigens45. This evidence concerns the gene CXCL12 and neoplasm.