{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nN6‐methyladenosine (m6A) is a widespread post‐transcriptional modification that regulates RNA fate, and VIRMA (also known as KIAA1429) represents the largest constituent of the m6A methyltransferase complex. Through its RNA binding domain, VIRMA orchestrates m6A deposition, influencing RNA splicing, processing, and stability. Aberrant expression of VIRMA has been documented in diverse pathological conditions including hepatocellular carcinoma, kidney cancers, lung adenocarcinoma, gastric malignancies, atherosclerosis, and germ cell tumors, highlighting its central role in modulating transcriptomic programs and supporting its potential as a biomarker in disease progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDetailed mechanistic investigations have revealed that VIRMA exerts its oncogenic influence by modulating the stability and translation of key transcripts. For instance, in breast, gastric, and lung cancers, VIRMA has been shown to affect the m6A modification of mRNAs encoding regulators such as CDK1, LINC00958 and DAPK3, as well as to control transcript stability via both m6A‐dependent and independent mechanisms (e.g., HK2 and long noncoding RNA networks like LINC00667). In nasopharyngeal carcinoma, intrahepatic cholangiocarcinoma, ovarian cancer, and Ewing sarcoma, VIRMA‐guided modifications fine‐tune the expression of oncogenes and tumor suppressors (such as E2F7, PTGS2, and components of circRNA axes), establishing intricate regulatory loops that drive tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond reprogramming RNA metabolism to favor tumorigenesis, VIRMA contributes to therapeutic resistance, cell death regulation, and metastatic progression. In lung adenocarcinoma and colorectal cancer, VIRMA‐mediated m6A modifications activate signaling cascades such as the JNK/MAPK pathway and mitigate ferroptotic cell death, thereby fostering radioresistance and chemoresistance. Moreover, its roles extend to head and neck and oral squamous cell carcinomas, as well as to hematologic malignancies like multiple myeloma, while emerging evidence also implicates VIRMA in developmental disorders including Hirschsprung’s disease. Collectively, these findings underscore VIRMA’s broad biological impact and validate its promise as a prognostic biomarker and therapeutic target across multiple clinical contexts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "João Lobo, Ana Laura Costa, Mariana Cantante, et al. 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