KRT17 is a type I keratin intermediate filament protein with diverse roles spanning epithelial homeostasis and disease pathogenesis. In normal physiology, KRT17 functions in hair follicle morphogenesis and is expressed in basal and wound-proximal keratinocytes, where it acts as a barrier alarmin promoting innate immune activation 1. KRT17 regulates epithelial proliferation through Akt/mTOR pathway signaling and modulates TNF function during hair cycling. In disease contexts, KRT17 exhibits context-dependent functions. In pulmonary fibrosis, KRT17+ epithelial cells represent a pathologic, ECM-producing population enriched in fibrotic lungs, and KRT17 expression marks dedifferentiated airway basal cells that promote fibroblast proliferation and extracellular matrix deposition 23. TGF-Ξ²1 signaling promotes transition to a KRT17+ basaloid epithelial state in IPF pathogenesis 4. Conversely, in colorectal cancer, KRT17 exerts protective immunity by promoting T-lymphocyte infiltration through YTHDF2-mediated CXCL10 upregulation, correlating with better clinical outcomes and immunotherapy response 5. In oral squamous cell carcinoma, KRT17 elevation drives cancer stemness and chemoresistance via integrin/FAK/Src/ERK/Ξ²-catenin signaling, while miRNA-485-5p suppression of KRT17 sensitizes tumors to chemotherapy 6. In psoriasis, KRT17+ keratinocytes co-localize with IL-23-producing dendritic cells and CD161+ IL-17+ T cells, suggesting involvement in autoimmune amplification 7.