PTGIS (prostaglandin I2 synthase) is a cytochrome P450 family member that catalyzes the isomerization of prostaglandin H2 to prostacyclin (PGI2), a potent vasodilator and platelet aggregation inhibitor 1. The gene is located on chromosome 20.11-q13.13 as a single copy per haploid genome 2 and contains a GC-rich promoter region responsive to shear stress and inflammatory signals 2. Beyond canonical eicosanoid metabolism, PTGIS displays dehydratase activity toward hydroperoxy-eicosatetraenoates [UniProt data]. Functionally, PTGIS-dependent PGI2 signaling regulates immune responses and tissue remodeling. In endometriosis, hypoxia-induced PTGIS overexpression promotes endometrial stromal cell adhesion and suppresses natural killer cell activity via PGI2 receptor (PTGIR) signaling 3. Conversely, in lung squamous cell carcinoma, low PTGIS expression correlates with poor prognosis and reduced immune infiltration 4. PTGIS shows tissue-protective roles in fibrotic diseases. In Crohn's disease, TGF-β suppresses PTGIS transcription, impairing antifibrotic PGI2-PTGIR signaling in intestinal fibroblasts 5. Similarly, PTGIS deficiency exacerbates renal fibrosis in chr20 kidney disease models, while PGI2 analogs mitigate fibrosis through fibroblast PTGIR activation 6. PTGIS was identified as a candidate gene for high-altitude adaptation in Tibetan populations 7.