Since MYC-driven tumours become addicted to CHK1 signalling, an important question arising from our studies was how the mutant NF-κB subunit Eμ-Myc lymphomas that are deficient in this signalling pathway are still able to survive, especially as both models display earlier onset of disease [18,24] (Supplementary Figure S1B). The gene discussed is MYC; the disease is lymphoma.