In murine models, combination therapy with CXCR4 antagonists and PD-1 blockade not only suppressed Tumor growth and prolonged survival but also reprogrammed intratumoral conventional type 1 DCs (cDC1s) with increased abundance and heightened functional activity, thereby enhancing CD8+ T cell priming and infiltration and restoring sensitivity to ICIs[170]. The gene discussed is CXCR4; the disease is neoplasm.