They found that in the SLN of breast cancer, the resident conventional DC subpopulation (LNR-cDC) showed suppressed activation (e.g., decreased CD86 expression) before the tumor had metastasized, and this suppression preceded the exhaustion of T-cell effector function, suggesting that the LNR-cDC may be a key target for breaking through immunosuppression and restoring anti-tumor immunity (7). The gene discussed is CD86; the disease is neoplasm.