Although previous studies discovered that CAML is essential for growth of activated immune cells,13,14,15 its function in mammalian TA insertion was only revealed more recently.8 For this study, we aimed to reconcile these distinct roles of CAML in cell viability and TA insertion using Eμ-Myc lymphoma cell lines with tamoxifen-inducible deletion of Caml. Our results indicate that CAML is required for the survival and growth of Myc-driven B-cell lymphomas, in culture and in vivo, likely by facilitating mitosis. The gene discussed is CAMLG; the disease is B-cell non-Hodgkin lymphoma.