NFKB1 and neoplasm: Consistently, HDAC5 silencing could improve ICB sensitivity by activating the NF-κB/PD-L1 axis in immunotherapy-resistant pancreatic tumors [144], demonstrating that the effectiveness of ICB depends on the high expression rate of PD-L1 of tumor cells and NF-κB activation could reverse ICB resistance by enhancing PD-L1 expression.