NFKB1 and neoplasm: These results suggest that the USP8 inhibitor treatment might reprogram an inflamed TME evidenced by upregulation of PD-L1 and activation of NF-κB to promote the gene expression of MHC-I presenting pathway, which enhances the tumor-infiltrating CD8+ cytotoxic T cells to enable the PD-1/PD-L1 blockade in vivo.