MMP17 (matrix metalloproteinase 17, also termed MT4-MMP) is a GPI-anchored membrane-type metalloproteinase that degrades extracellular matrix components and mediates proteolytic activation of inflammatory mediators 1. The enzyme cleaves pro-TNF at the '74-Ala-|-Gln-75' site and is implicated in ADAMTS4 aggrecanase activation, particularly in inflammatory cartilage degradation 2. MMP17 does not hydrolyze collagen types I-V, gelatin, fibronectin, or laminin. In inflammatory osteoarthritis, MMP17 mediates IL-1β-induced aggrecan degradation and glycosaminoglycan loss, with MMP17 null mice showing protection against inflammatory but not mechanical cartilage injury 2. Clinically, MMP17 expression is significantly elevated across multiple malignancies. In epithelial ovarian cancer, high MMP17 expression independently predicts poor overall survival, progression-free interval, and disease-specific survival, with an AUC of 0.988 for cancer diagnosis 3. MMP17 is also highly expressed in sinonasal mucosal melanoma (64.52% of cases) 4 and shows promise as a prognostic biomarker in endometrial carcinoma 5. In Kawasaki disease with coronary artery lesions, myeloid cells upregulate MMP17 alongside other proteases, contributing to vascular injury 6. MMP17 inhibition by doxycycline suppresses rhabdoid tumor progression through PI3K-Akt pathway suppression 7. These findings establish MMP17 as a key regulator of ECM homeostasis with disease relevance spanning inflammation, cancer progression, and cardiovascular complications.