Further evidence for this Pim/MYC collaboration and MYC dependence on Pim expression for oncogenesis is provided by observation of longer latency to development of lymphoma in Pim knockout mice.11 In support of redundancy of Pims in hematological malignancy, upregulation of Pim-2 in Pim-1-deficient mice and Pim-3 in Pim-1/Pim-2-deficient mice with preserved lymphomagenesis is observed.11 Here, PIM2 is linked to lymphoma.