BLM is complexed with Topoisomerase III alpha, RMI1, and RMI2 (Meetei et al., 2003), and this complex has the unusual capacity to disentangle double Holliday junctions by dissolution (Wu and Hickson, 2003; Raynard et al., 2006; Wu et al., 2006), which led to the interesting proposal that the high sister-chromatid exchange phenotype of Bloom syndrome cells could be accounted for by a default mechanism for double-Holliday-junction resolution that involved breakage and rejoining in the absence of the BLM complex. This evidence concerns the gene BLM and Bloom syndrome.