Tumor-derived CSF-1 controlled the quantity of CSF-1R+CD11c+ myeloid-derived suppressor cells (MDSCs) and the infiltration of activated CD8+ T cells into the tumor, which subsequently affected the sensitivity to the FDA-approved immunotherapy for HNC, anti-PD-1 (αPD-1).20 We showed that the timing of αPD-1 supplementation to trametinib treatment is crucial, as tumor elimination occurred only when αPD-1 supplementation was administered in the time window during which trametinib treatment had temporarily reduced CSF-1 expression and induced an immune active TME. The gene discussed is CSF1R; the disease is neoplasm.