CTLA4 and neoplasm: Pre-treatment with IFN-γ, the TLR3 ligand poly (I:C), and anti-IL-10 Ab, which attract IFN-γ-producing NK cell infiltration into tumor sites, rendered tumors sensitive to checkpoint blockade therapy (e.g., mAbs recognizing CTLA-4 and PD-1), leading to increased cure rates.