The programmed cell death-1 (PD-1) and programmed death ligand-1 (PD-L1) have exhibited a potent response in various tumors such as triple-negative breast cancer (TNBC); however, only a small portion of TNBC patients respond to ICT because of the immunosuppressive tumor microenvironment (TME) and immunologically “cold” tumors, which later show low mutational load, lack of T-cell infiltration, deficient PD-L1, and low MHC I expressions. Here, PDCD1 is linked to neoplasm.