In our study, we found that HLA-G desensitizes breast cancer cells to trastuzumab by binding to the NK-cell receptor KIR2DL4 and the blockade of HLA-G/KIR2DL4 axis improves the vulnerability of HER2-positive breast cancer to trastuzumab treatment in vivo (134). The gene discussed is ERBB2; the disease is breast cancer.