However, using B cell specific Chk1 knock-out mice we could show that Eμ-MYC driven tumors highly depend on CHK1 as none of our Mb1-Cre Chk1fl/− mice expressing the MYC transgene developed cancer over an observation period of one year and disease onset was found delayed in Chk1+/− mice. The gene discussed is MYC; the disease is cancer.