RNAi screening identified TBK1 as a protein whose function is required for the survival of cancer cells which harbor activated K-RAS, implicating TBK1 and activated K-RAS as synthetic-lethal partners (i.e. KRAS-activating mutations are expected to sensitize the cells harboring them to TBK1 inhibition) [16]. This evidence concerns the gene TBK1 and cancer.