RMI1 (RecQ-mediated genome instability 1) is an essential component of the BTR complex (BLM-TOP3A-RMI1/2), which plays a critical role in DNA recombination intermediate processing and genome stability. Mechanistically, RMI1 promotes TOP3A binding to double Holliday junctions and stimulates their dissolution, preventing aberrant DNA crossover formation 1. The RMI1-containing complex also regulates mitotic telomere deprotection through coordinate action with the chromosome 9 complex, enabling controlled telomere DNA damage responses 2. RMI1 is required for BLM and TOP3A stability and participates in DNA replication fork resolution at telomeres 34. Disease relevance includes genome instability disorders and cancer. RMI1 knockdown enhances radiosensitivity and apoptosis following ionizing radiation exposure, with altered circRNA expression patterns affecting mismatch repair and apoptotic pathways 5. Additionally, RMI1 deficiency confers obesity resistance through altered adipocyte hyperplasia regulation, suggesting roles in metabolic homeostasis beyond DNA repair 6. RMI1 was identified as a diagnostic hub gene in atherosclerosis with rheumatoid arthritis comorbidity 7. Clinically, RMI1 dysfunction associates with increased chromosome 9 and genomic instability, with potential implications for cancer treatment strategies targeting DNA repair pathways 3.