In summary, our results suggest that the pseudogene HLA-DPB2 may act as an endogenous RNA to adsorb has-miR-370-3p and upregulating its parental gene HLA-DPB1, thereby recruiting more TILs into the tumor microenvironment and increasing the expression of PD-1, PD-L1, and CTLA-4 in BC tissues, ultimately improving the prognosis of BC patients. The gene discussed is CTLA4; the disease is neoplasm.