In this context, the short-term duration and reduced response in TNBC patients treated with immune checkpoint inhibitors (ICB) could be partly due to the upregulation of different immune-escape biological mechanisms in the CSC subset and to the heterogeneous expression of PD-L1 in TNBC differentiated/bulk tumor cells, which could, in turn, function as “decoys” for ICB activity by decreasing their efficacy over the less frequent CSC compartment. Here, CD274 is linked to neoplasm.