Multiple mechanisms of acquired resistance to EGFR inhibitors have been reported, including a secondary “gatekeeper” mutation in EGFR (T790M) [6], MET receptor gene amplification [7], the activation of TGF-β, NF-κB, or IGFIR signaling [8–10], or the pathological transformation of NSCLC to small cell lung cancer (SCLC), etc [11–12]. This evidence concerns the gene NFKB1 and small cell lung carcinoma.