In an interesting study that tested timing of checkpoint therapy administration, targeting PD-1 is only effective when given very early after tumor initiation, unless CXCR2 signaling is blocked; with CXCR2 blockade, there is lower myeloid-derived suppressor cell infiltration into the TME, which restores the efficacy of subsequently initiated anti-PD-1 therapy against tumor growth (78). This evidence concerns the gene CXCR2 and neoplasm.