PGAP3 is a glycosylphosphatidylinositol (GPI) phospholipase involved in the fatty acid remodeling steps of GPI-anchor maturation, where it likely catalyzes the removal of unsaturated acyl chains at sn-2 of inositol phosphate to generate lyso-GPI intermediates 1. This remodeling process is critical for proper integration of GPI-anchored proteins into lipid rafts. PGAP3 is located on chromosome 17-21, a region highly linked to asthma susceptibility 2. The gene shows increased expression in asthmatic airway smooth muscle cells compared to non-asthmatic controls, and when overexpressed, it enhances cell proliferation, contractility, and expression of asthma-associated genes including GATA3 and ALOX5 3. In bronchial epithelial cells, PGAP3 regulates antiviral genes such as RSAD2, OASL, and IFN-λ, suggesting a role in respiratory virus responses linked to asthma exacerbations 2. Biallelic pathogenic variants in PGAP3 cause PGAP3-CDG, a congenital disorder of glycosylation characterized by developmental delay, intellectual disability, seizures, hyperphosphatemia, brain malformations, and characteristic facial features 4. The gene also shows co-amplification with ERBB2 in gastric cancer, contributing to tumor progression and poor prognosis 5.