In addition, blocking HLA-G/KIR2DL4 enhanced the toxicity of NK cells to cocultured colorectal cancer cells induced by cetuximab, a monoclonal antibody against the epidermal growth factor receptor (EGFR), suggesting a common role of HLA-G/KIR2DL4 signaling in repressing ADCC in cancer immunotherapy (Supplementary Fig. S8a, b).28 Thus, HLA-G/KIR2DL4 mediates an interaction between malignant cells and NK cells resulting in repression of therapeutic antibody-triggered ADCC. This evidence concerns the gene EGFR and cancer.