PIM2 is a serine/threonine kinase proto-oncogene that functions as a central regulator of cell survival and proliferation through multiple interconnected mechanisms. Structurally localized to the cytoplasm, PIM2 exerts its oncogenic activity primarily through phosphorylation-mediated effects on key cellular targets 1. The kinase directly phosphorylates metabolic enzymes including PGK1, PDHA1, and PFKFB2/PFKFB4, promoting aerobic glycolysis reprogramming—a hallmark of cancer-like metabolic changes 21. PIM2 stabilizes the MYC oncoproteins and regulates cell cycle progression through phosphorylation of cyclins and CDK inhibitors (CDKN1A, CDKN1B). It suppresses apoptosis via phosphorylation of BAD and activates survival signaling through the NF-κB pathway via MAP3K8/COT phosphorylation 3. Additionally, PIM2 promotes autophagy and regulates chondrocyte survival in epiphyseal growth plates 4. PIM2 is overexpressed in multiple hematological malignancies including multiple myeloma and acute myeloid leukemia, where its constitutive kinase activity is tightly controlled by proteasomal degradation rather than ubiquitination 3. Clinically, PIM2 represents a therapeutic target; proteasome inhibitors and PIM2-specific inhibitors demonstrate additive effects in suppressing myeloma growth 3. Recent evidence links PIM2 to inflammatory arthritis, Crohn's disease comorbidity, and breast cancer prognosis 256.