BLM (Bloom syndrome helicase) is a RecQ family DNA helicase essential for maintaining genomic stability through multiple DNA repair mechanisms. The protein functions primarily in homologous recombination repair, forming the BTR complex with topoisomerase IIIα, RMI1, and RMI2 to dissolve double Holliday junctions and prevent chromosome 15 1. BLM exhibits 3'-5' helicase activity and processes various DNA substrates including four-way junctions, G-quadruplexes, and replication fork intermediates. At telomeres, BLM plays a crucial role in alternative lengthening of telomeres (ALT) by unwinding lagging strand substrates to assemble DNA damage responses 2. The protein also functions in telomere protection by promoting D-loop unwinding and inhibiting aberrant homology-directed repair when recruited by TRF2-RAP1 3. BLM stability is regulated by USP37-mediated deubiquitination, which is enhanced following DNA damage 4. Loss-of-function mutations in BLM cause Bloom syndrome, a genetic disorder characterized by growth retardation, immunodeficiency, and cancer predisposition. In cancer contexts, BLM is overexpressed in glioblastoma and contributes to chemotherapy resistance, with BLM-depleted cells showing increased sensitivity to DNA-damaging agents 54.