In addition, NFκB, a downstream mediator of mutant Kras signaling in PDAC [17, 18], was found to be constitutively activated in most primary pancreatic cancers and cell lines [19, 20], due partly to the overexpression of β-TrCP [21], a F-box protein of SCF E3 ligase that promotes degradation of IκB [22] to activate NFκB and DEPTOR to activate mTORC1/2 [6–8]. This evidence concerns the gene NFKB1 and pancreatic neoplasm.