Authors also showed that a specific target, such as NF-KB, was inactivated in animal tumors pretreated with thymoquinone followed by gemcitabine and/or oxaliplatin, thus suggesting that thymoquinone could abrogate gemcitabine or oxaliplatin-induced activation of NF-KB, resulting in the chemosensitization of pancreatic tumors to conventional therapeutics [35]. Here, NFKB1 is linked to pancreatic neoplasm.