Taken together with our previous analysis of down-regulated (phospho)proteins [20], these data demonstrate that Eμ-Myc/cRel−/− lymphomas have undergone significant rewiring of their signalling pathways, specifically hyper-activation of the PI3K/AKT and ERK pathways, which are known to inhibit apoptosis and cell cycle arrest [44,45], potentially explaining how these tumours are surviving loss of CHK1. The gene discussed is CHEK1; the disease is neoplasm.