The immunosuppressive TME can exploit antitumor immune responses and inhibit CD4+ and CD8+ T cells, leading to eventual escape of HER2pos BC cells from immune surveillance.21 Prominent efforts have been made in recent years to develop immunotherapies to aid HER2-targeted therapies, modulate the immunosuppressive TME, and improve clinical outcomes in patients with HER2pos BC. The gene discussed is CD8A; the disease is breast cancer.