Thus, we speculate that NK cells could play a role in mediating a later-stage antimetastatic T cell immune response, either by recruiting DC1 by secreting CXCL1 (as is documented in other tumor models [42]) or by triggering the production of IFN-γ-inducible chemokines such as CXCL9 and CXCL10, critical for recruitment of effector T cells. This evidence concerns the gene CXCL1 and neoplasm.