The working hypothesis of the current manuscript is that the CXCR3-CXCL9/10 axis is a key driver of effector and cytotoxic CD4+ and CD8+ T cell function and that this axis maintains a self-feeding amplification loop in which the interaction of CXCL9 and CXCL10 with CXCR3 induces different subtypes of effector and cytotoxic CD4+ and CD8+ T cells with an IFNγ signature; since CXCL10 is IFNγ inducible (31, 32), high levels of IFNγ then further induces CXCL10 production, not only by T cells but also by cancer cells, thus reinforcing the loop. The gene discussed is CXCR3; the disease is cancer.