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Gene set variation analysis was conducted to characterise hallmark pathway gene signatures, and single\u2010cell regulatory network inference and clustering were utilised to analyse transcription factor regulons. Immunohistochemistry and immunofluorescence were performed to validate cellular components of PA tissues. siRNA knockdown and gene overexpression, alongside quantitative polymerase chain reaction, Western blotting and cell proliferation assays, were conducted for functional investigations.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>There was a pervasive increase in gene transcription in PA cells (PACs) compared with PG cells. This is associated with high expression of histone\u2010lysine N\u2010methyltransferase 2A (KMT2A). High KMT2A levels potentially contribute to promoting PAC proliferation through upregulation of the proto\u2010oncogene <jats:italic>CCND2<\/jats:italic>, which is mediated by the transcription factors signal transducer and activator of transcription 3 (STAT3) and GATA binding protein 3 (GATA3). PA tissues are heavily infiltrated with myeloid cells, while fibroblasts, endothelial cells and macrophages in PA tissues are commonly enriched with proinflammatory gene signatures relative to their counterparts in PG tissues.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>We revealed the previously underappreciated involvement of the KMT2A\u2012STAT3\/GATA3\u2012<jats:italic>CCND2<\/jats:italic> axis and chronic inflammation in the pathogenesis of PA. These findings underscore the therapeutic promise of KMT2A inhibition and anti\u2010inflammatory strategies, highlighting the need for future investigations to translate these molecular insights into practical applications.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Single\u2010cell RNA\u2010sequencing reveals a transcriptome catalogue comparing sporadic parathyroid adenomas (PAs) with normal parathyroid glands.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>PA cells show a pervasive increase in gene expression linked to KMT2A upregulation.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>KMT2A\u2010mediated STAT3 and GATA3 upregulation is key to promoting PA cell proliferation via cyclin D2.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>PAs exhibit a proinflammatory microenvironment, suggesting a potential role of chronic inflammation in PA 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