Pim-1, 2 and 3 (EC 2.7.11.1) make up a distinct and highly homologous family of serine/threonine kinases belonging to the Ca2+/calmodulin-dependent protein kinase-related (CAMK) family. Pim proteins are widely expressed with high levels in hematopoietic tissue and are aberrantly expressed in a variety of human malignancies. These proteins are considered to be constitutively active and, therefore, regulated by expression and proteosomal degradation. Gene transcription is initiated by a wide range of cytokines, mitogens and growth factors that transduce signals via the Janus kinase-signal transducers and regulators of transcription (JAK/STAT pathway), thereby regulating Pim expression[1]. Pim kinases play a major role in cell cycle regulation, anti-apoptotic activity and the homing and migration of receptor tyrosine kinases mediated via the JAK/STAT pathway. The discovery of these kinases being up-regulated in many hematological malignancies and solid tumors affords them therapeutic opportunities in oncology[2].