Indeed, when the PD-L1 or PD-1 induced signaling is affected, as in the case of treatment with antagonistic mAbs, the tumor cells seem to perceive this ligand/receptor unavailability and respond by activating NF-kB hyperphosphorylation, provoking its translocation into the nucleus and likely PD-1 and PD-L1 or CSN5 transcription (see Figure 3B). This evidence concerns the gene NFKB1 and neoplasm.