Finally, DCs have been found to increase the production of CXCL9 and CXCL10 in an IFN-γ-dependent manner, which facilitates the infiltration of CD8+ T cells into tumors.43 Consistently, we also demonstrated that cDC1 in the TME produced more CXCL9 to recruit effector CD8+ T cells into TME through CXCL9-CXCR3 axis after inhibition of BCL9, supporting that targeting Wnt/β-catenin signaling promotes the tumor infiltration of CD8+ T cells. Here, CXCR3 is linked to neoplasm.