In sum, T-αFGL2 therapy induced tumor-reactive T cell proliferation, promoted secretion of granzyme B to control tumor progression, and increased CXCR3 and CD69 expression on CD8+ TM cells to facilitate their brain retention, which fostered the formation of tumor-specific brain-resident CD8+ TRM cells (Fig. 8h). The gene discussed is CXCR3; the disease is neoplasm.