Activation of K-Ras by mutation, or other means, renders non-small cell lung cancer (NSCLC) cells ‘addicted’ to the presence of TBK1 (TANK-binding kinase 1) protein for continued proliferation and/or survival [1], possibly via direct stimulation of TBK1 activity [2]. The gene discussed is TBK1; the disease is non-small cell lung carcinoma.