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Disease category was assigned by treating physicians. Clinical data and autoantibody profiles were collected. RNA was sequenced using the Illumina NextSeq 500 platform. Differentially expressed genes (DEGs) were identified using Partek Flow and DESeq2, applying a log\n                      <jats:sub>2<\/jats:sub>\n                      fold change cutoff of \u00b11.5 and a false discovery rate of &lt;0.1.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Patients with jOverlap, predominantly White girls, had distinct autoantibody patterns enriched for PM\u2010Scl, U1\u2010RNP, and U3\u2010RNP. Compared to HCs, patients with jSSc, JDM, and jOverlap demonstrated a unique gene expression profile, with up\u2010regulation of type\u20101 interferon\u2010related genes, specifically\n                      <jats:italic>SIGLEC1<\/jats:italic>\n                      and\n                      <jats:italic>IFI27<\/jats:italic>\n                      . Compared to patients with JDM, patients with jOverlap showed higher expression of\n                      <jats:italic>RAB13<\/jats:italic>\n                      (linked to sclerosing neurodegenerative disease),\n                      <jats:italic>MMEL1<\/jats:italic>\n                      (inflammatory arthritis), and\n                      <jats:italic>MMP19<\/jats:italic>\n                      (pulmonary fibrosis). t\u2010distributed stochastic neighbor embedding clustering revealed that although HC, jSSc, and JDM samples each formed distinct clusters, jOverlap samples were distributed across all clusters, highlighting their heterogeneity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Patients with jOverlap exhibited a distinct immunophenotype and clinical profile compared to patients with jSSc and JDM. Their broad transcriptional heterogeneity suggests disease category alone does not explain gene expression patterns. Further analysis correlating DEGs with autoantibodies, age, and clinical features is warranted to better define this overlapping disease entity.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/acr290005-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/acr2.90005","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T16:58:20Z","timestamp":1772989100000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Distinct by Design: Unraveling the Unique Clinical and Transcriptomic Identity of Juvenile Scleromyositis Overlap Compared to Juvenile Systemic Sclerosis and Juvenile Dermatomyositis: Implications for Care and Pathogenesis"],"prefix":"10.1002","volume":"8","author":[{"given":"Amanda D.","family":"Robinson","sequence":"first","affiliation":[{"name":"Pediatric Rheumatology University of Utah  Salt Lake City"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Clare E.","family":"Pain","sequence":"additional","affiliation":[{"name":"Pediatric Rheumatology Alder Hey Children's NHS Foundation Trust  Liverpool United Kingdom"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4058-7112","authenticated-orcid":false,"given":"Gabrielle A.","family":"Morgan","sequence":"additional","affiliation":[{"name":"Pediatric Rheumatology Ann &amp; Robert H. 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