PIM1 is a serine/threonine kinase proto-oncogene that functions as a key regulator of cell survival and proliferation, conferring selective advantages in tumorigenesis 1. The kinase exerts oncogenic activity through multiple interconnected mechanisms: phosphorylation and stabilization of MYC to enhance its transcriptional activity, inhibition of pro-apoptotic proteins (BAD, MAP3K5, FOXO3) to suppress apoptosis, and promotion of cell cycle progression via phosphorylation of CDC25A/C and CDKN1A/B 23. Beyond canonical oncogenic pathways, PIM1 acts as a positive regulator of mTORC1 signaling through DEPDC5 phosphorylation and negatively regulates innate immunity by inactivating GBP1, preventing unwanted immune damage 45. Recent evidence reveals PIM1's broader pathological significance: it promotes endothelial-to-mesenchymal transition via NDRG1 phosphorylation, contributing to atherosclerosis progression 6; drives myofibroblast ferroptosis resistance in skin fibrosis diseases 7; and regulates T helper cell differentiation through the AKT/FOXO1 pathway in autoimmune uveitis 8. PIM1 overexpression is implicated in both hematologic and solid malignancies, positioning it as an emerging therapeutic target 910. PIM1 inhibition demonstrates promise in suppressing cancer cell proliferation and modulating pathologic immune responses across multiple disease contexts.