Given the above mentioned data linking KRAS to activation of the canonical IKK complex in lung cancer, and given that we had previously shown that increased NF-κB activity in KRAS-driven mouse lung tumors were associated with increased phosphorylation of IκBα, and that KRAS-induced NF-κB activity in lung cells required IKKβ [23], the main catalytic subunit of the canonical IKK complex, we hypothesized that a reasonable druggable target in the KRAS-induced NF-κB activation pathway in lung cancer would be the IKKβ kinase. This evidence concerns the gene NFKB1 and lung carcinoma.