By surface plasmon resonance assay, Liu et al. revealed a previously unrecognized antitumor mechanism of BBR: it could interact with CSN5 directly (KD = 16.25 mM) to inhibit its deneddylase activity, therefore triggering the proteasome-dependent degradation of PD-L1 and activating the tumor-infiltrating T cells [175]. Here, CD274 is linked to neoplasm.