In this regard, oncogenic KRAS is known to cooperate with pro-inflammatory nuclear factor (NF)-κB signaling in cancer cells to drive stemness, pro-inflammatory mediator elaboration, and responsiveness to IL-1β signaling [8,9,10,11], and is ideally positioned as a biomarker of therapeutic response to anti-IL-1β therapy. This evidence concerns the gene NFKB1 and cancer.