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Due to its poorly understood pathophysiology and lack of specific biomarkers, diagnosis is frequently delayed. Understanding FPIES genetics can shed light on disease susceptibility and pathophysiology\u2014key to developing diagnostic, prognostic, preventive and therapeutic strategies. Using a well\u2010characterised cohort of patients we explored the potential genome\u2010wide susceptibility factors underlying FPIES.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Blood samples from 41 patients with oral food challenge\u2010proven FPIES were collected for a comprehensive whole exome sequencing association study.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Notable genetic variants, including rs872786 (<jats:italic>RBM8A<\/jats:italic>), rs2241880 (<jats:italic>ATG16L1<\/jats:italic>) and rs2289477 (<jats:italic>ATG16L1<\/jats:italic>), were identified as significant findings in FPIES. A weighted SKAT model identified six other associated genes including <jats:italic>DGKZ<\/jats:italic> and <jats:italic>SIRPA<\/jats:italic>. DGKZ induces TGF\u2010\u03b2 signalling, crucial for epithelial barrier integrity and IgA production; <jats:italic>RBM8A<\/jats:italic> is associated with thrombocytopenia absent radius syndrome, frequently associated with cow's milk allergy; <jats:italic>SIRPA<\/jats:italic> is associated with increased neutrophils\/monocytes in inflamed tissues as often observed in FPIES; <jats:italic>ATG16L1<\/jats:italic> is associated with inflammatory bowel disease. Coexpression correlation analysis revealed a functional correlation between <jats:italic>RBM8A<\/jats:italic> and filaggrin gene (<jats:italic>FLG<\/jats:italic>) in stomach and intestine tissue, with filaggrin being a known key pathogenic and risk factor for IgE\u2010mediated food allergy. A transcriptome\u2010wide association study suggested genetic variability in patients impacted gene expression of <jats:italic>RBM8A<\/jats:italic> (stomach and pancreas) and <jats:italic>ATG16L1<\/jats:italic> (transverse colon).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>This study represents the first case\u2013control exome association study of FPIES patients and marks a crucial step towards unravelling genetic susceptibility factors underpinning the syndrome. Our findings highlight potential factors and pathways contributing to FPIES, including epithelial barrier dysfunction and immune dysregulation. While these results are novel, they are preliminary and need further validation in a second cohort of patients.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.14564","type":"journal-article","created":{"date-parts":[[2024,9,30]],"date-time":"2024-09-30T22:56:19Z","timestamp":1727736979000},"page":"919-929","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Whole Exome Sequencing Identifies Epithelial and Immune Dysfunction\u2010Related Biomarkers in Food Protein\u2010Induced Enterocolitis Syndrome"],"prefix":"10.1111","volume":"54","author":[{"given":"Alba","family":"Camino\u2010Mera","sequence":"first","affiliation":[{"name":"Genetics, Vaccines and Infections Research Group (GenViP), Instituto de Investigaci\u00f3n Sanitaria de Santiago Universidade de Santiago de Compostela  Santiago de Compostela Galicia Spain"},{"name":"Unidade de Xen\u00e9tica, Instituto de Ciencias Forenses, Facultade de Medicina Universidade de 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