Pim genes were originally identified as oncogenes in mouse models in the 1980s, and were found to encode serine/threonine kinases with a broad range of cellular targets. Pim kinases have unique structural properties, and are characterized by a constitutive serine/threonine kinase activity that does not depend on post-translational modifications for activation. Pim kinases are potent oncogenes and are overexpressed in a range of haematopoietic malignancies and solid cancers. The oncogenic properties of Pim kinases were shown to encompass their capacity to counteract the increased sensitivity to apoptosis induction that is associated with MYC-driven tumorigenesis. Recent progress has characterized the survival signalling of the Pim family of oncogenic serine/threonine kinases in considerable detail. In this Review, we provide a discussion of the physiological functions of Pim kinases and consider the main mechanisms by which PIM exerts its oncogenic activities: through the regulation of MYC transcriptional activity; the regulation of cap-dependent protein translation; the regulation of cell cycle progression; and through survival signalling by phosphorylation of BAD. We conclude this Review by briefly exploring the opportunities for therapeutic interventions that are aimed at the inhibition of Pim kinases.