Both CXCL9 and CXCL10 induced rapid proliferation (ki-67) and IL-2 production by both CD4+ and CD8+ T cells, with a marked increase in tumor-specific (TRP2-specific) CD8+ T cells, and an increase in granzyme-B+ CD4+ T cells, which may explain in part the efficacy of the adoptive transfer studies in which CXCL10-Fc and CXCL9-Fc limit tumor progression in CXCR3KO mice that are reconstituted with CXCR3+ CD4+ T cells (Figure 6B). The gene discussed is MKI67; the disease is neoplasm.