IL11 (interleukin 11) is a pro-inflammatory cytokine of the IL-6 family that plays crucial roles in fibrosis, aging, and disease pathogenesis. Originally identified as a hematopoietic factor supporting megakaryocyte colony formation and platelet production 1, recent research reveals IL11 is largely redundant for hematopoiesis and instead promotes pathological processes 2. IL11 signals through JAK/STAT3, ERK/P90RSK, LKB1/mTOR and GSK3β/SNAI1 pathways in autocrine and paracrine fashion, activating mesenchymal transition programs that drive inflammation and fibrosis 2. The protein is a dominant transcriptional response to TGFβ1 in fibroblasts and is required for pro-fibrotic effects, causing heart and kidney fibrosis through non-canonical ERK-dependent signaling 3. IL11 expression increases with aging across tissues, regulating ERK-AMPK-mTORC1 pathways to promote age-related pathologies 4. In disease contexts, IL11 promotes epithelial-to-mesenchymal transition, prevents beneficial alveolar regeneration in lung disease 5, drives cardiac fibrosis through macrophage-to-myofibroblast transition 6, and supports tumor invasion and metastasis via STAT3 signaling 7. Importantly, genetic deletion or therapeutic inhibition of IL11 signaling extends lifespan and protects against multiple age-related diseases 4.