described another interesting mechanism in which TAMs, after neoadjuvant treatment with the anti-HER2 humanized antibody trastuzumab, develop an immunosuppressive phenotype, upregulating B7-H4, a member of the B7 family of T cell costimulatory molecules, and causing the immune escape of HER2-positive BC cells (72). The gene discussed is VTCN1; the disease is breast cancer.