Preclinical studies have demonstrated that tumor-specific T helper type-1 (Th1) and T cytotoxic type-1 (Tc1) cells, but not type-2 counterparts, can efficiently traffic into CNS tumor sites and mediate effective therapeutic efficacy, recruited via the type-1 chemokine CXCL10 [1-3] and the integrin receptor, Very Late Antigen (VLA)-4 [4-7]. Here, CXCL10 is linked to neoplasm.