Finally, since PD-1/PD-L1 interaction is only one of many pathways exploited by anti-tumor immunity, it seems unlikely that one sole biomarker could sufficiently predict clinical response to immune checkpoint inhibitors in different treatment settings[131], particularly in the neoadjuvant setting where efficacy signals from checkpoint inhibition in TNBC appear to be irrespective of PD-(L)1 immunostaining status. The gene discussed is CD274; the disease is neoplasm.