The T-αFGL2 treatment boosts the CD69+CD62L−CD8+ T cell population, and this effect is abolished upon either depletion of the CXCR3 ligands CXCL9/10 or knockout of CXCR3 in the host mice, revealing an unanticipated link between CXCL9/10-CXCR3 signaling and tumor-specific CD8+ TRM cell formation in brains. The gene discussed is CD8A; the disease is neoplasm.