To define the role of mutant KRAS in the aberrant NF-κB activation patterns of KRASMUT tumor cells, including non-canonical endogenous NF-κB activity, resistance to IKKβ inhibition, and IL-1β-inducibility, we undertook short hairpin RNA (shRNA)-mediated KRAS silencing (shKras) and plasmid-mediated overexpression of a mutant dominant-negative form of ΙκΒα (pΙκΒαDN; inhibits canonical NF-κΒ signaling) in KRASMUT cell lines, as well as plasmid-mediated overexpression of mutant KRAS (pKrasG12C) in KRASWT cell lines11,33. This evidence concerns the gene IL1B and neoplasm.