Studies in vivo have used the classical urethane (Stathopoulos et al, 2007; Kelly-Spratt et al, 2009) or the conditional K-Ras–induced murine models of lung carcinogenesis, in which canonical NF-κB was suppressed using an IκBαSR super-repressor (Stathopoulos et al, 2007; Meylan et al, 2009) or by ablation of RelA/p65 (Basseres et al, 2010) or IKKβ (Xia et al, 2012), which led to reduced proliferation of K-RasG12D–induced lung adenocarcinomas in mice. The gene discussed is KRAS; the disease is lung adenocarcinoma.