A variety of nonmalignant cell types in the TME can also affect the occurrence, development, metastasis, and treatment response of BC; however, the majority of the genetic mechanisms that contribute toward patient outcomes remain unclear [10].Previous studies have demonstrated that the proliferation and metastasis of tumor cells are affected by immune cells and their mechanisms of action [11], including tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), CD4 + Th1 cells, CD8 + T cells, regulatory T cells (Tregs), and TH17 cells [12]. This evidence concerns the gene CD4 and neoplasm.