Activation of canonical NF-κB in response to EGFR oncogene inhibition in mutant EGFR-bearing human and mouse lung cancer cells, drives tumour cell survival and residual disease in lung cancer via several established regulators of canonical NF-κB signalling and cell survival such as TNFAIP3 (TNFα-induced protein 3), BIRC3 (c-IAP2, TNFR2-TRAF signalling complex protein) and IL-6 [16]. The gene discussed is EGFR; the disease is neoplasm.