KIR3DL1 and cancer: Preclinical data suggest that NGM707 stimulates myeloid and lymphocyte activation by blocking LIRB1 and reprograms inhibitory myeloid cells to a stimulatory state by blocking LIRB2.371 The HLA-B57-Fc fusion protein iosH2 binds to LILRB1/2 and KIR3DL1 with high affinity and blocks the binding of HLA-G and ANGPTL to LILRB1/2, promoting the conversion of macrophage in the M2 phenotype to the M1 phenotype and thus enhancing phagocytosis of cancer cells in vitro; iosH2 also increases the cytotoxicity of T cells and NK cells in coculture with cancer cell lines.372