The Pim family of serine/threonine kinases are named for their mode of discovery as proviral common integration sites in moloney murine leukemia virus (mMuLV)-induced lymphomas.8 Insertional mutagenesis screening utilizes transforming retroviruses to identify oncogenes overexpressed by the activity of the retroviral enhancer sequence.9 Cloning of retroviral integration sites in mMuLV-induced lymphomas led to the discovery of Pim-1 in the 1980s8 followed by Pim-210 and later Pim-3 in the 1990s in the screening of Pim-1/Pim-2 knockout models.11 This evidence concerns the gene MARK2 and lymphoma.