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However, the exact components and mechanisms of this shared genetic structure remain poorly understood. Here we show that\n                    <jats:italic>ROMO1<\/jats:italic>\n                    is a key shared genetic component among RA, MS, and T1D. Using differential gene expression (DGE) and LASSO regression analyses of bulk RNA-seq data from whole blood tissues, we identified\n                    <jats:italic>ROMO1<\/jats:italic>\n                    as a potential shared genetic factor. A multi-sample analysis with external Gene Expression Omnibus (GEO) data revealed\n                    <jats:italic>ROMO1\u2019s<\/jats:italic>\n                    consistent association with immune cell patterns across tissues in all three diseases. Single-gene Gene Set Enrichment Analysis (GSEA) suggested\n                    <jats:italic>ROMO1\u2019s<\/jats:italic>\n                    involvement in the reactive oxygen species (ROS) pathway, which was further substantiated by conjoint analysis with 256 ROS pathway-related genes(ROSGs) from Molecular Signatures Database (MSigDB). Single-gene Receiver Operating Characteristic (ROC) analysis highlighted\n                    <jats:italic>ROMO1\u2019s<\/jats:italic>\n                    potential as a disease biomarker. Single-cell RNA sequencing (scRNA-seq) analysis showed significantly altered\n                    <jats:italic>ROMO1<\/jats:italic>\n                    expression in monocytes and other immune cells compared to healthy control (HC). Immune infiltration analysis revealed\n                    <jats:italic>ROMO1\u2019s<\/jats:italic>\n                    significant association with monocytes across all three diseases. Furthermore, two-sample Mendelian randomization (MR) analysis using genome-wide association studies (GWAS) data demonstrated that\n                    <jats:italic>ROMO1<\/jats:italic>\n                    could regulate epitopes on monocytes, potentially lowering autoimmune disease risk. Our findings clarify the importance of\n                    <jats:italic>ROMO1<\/jats:italic>\n                    in the shared genetic architecture of RA, MS, and T1D, and its underlying mechanism in disease development.\n                  <\/jats:p>","DOI":"10.1007\/s10142-025-01598-x","type":"journal-article","created":{"date-parts":[[2025,4,20]],"date-time":"2025-04-20T21:54:17Z","timestamp":1745186057000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["A Multi-omics approach to identify and validate shared genetic architecture in rheumatoid arthritis, multiple sclerosis, and type 1 diabetes: integrating GWAS, GEO, MSigDB, and scRNA-seq data"],"prefix":"10.1007","volume":"25","author":[{"given":"Tailin","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"He","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kei Hang Katie","family":"Chan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,4,21]]},"reference":[{"issue":"10","key":"1598_CR2","doi-asserted-by":"publisher","first-page":"e30762","DOI":"10.7759\/cureus.30762","volume":"14","author":"C Almeida","year":"2022","unstructured":"Almeida C, Venade G, Duarte D, Vaz A, Nascimento E (2022) Type 1 diabetes mellitus and multiple sclerosis: an association to consider. 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