Interestingly, Eμ-Myc cRel−/− lymphomas have significant up-regulation of a pathway involving PI3K and AKT kinases, which are known to inhibit apoptosis and promote cell survival, providing an elegant model to explain how these cells, which lack Chk1 protein, can survive elevated levels of replication stress [10]. The gene discussed is CHEK1; the disease is lymphoma.