Increased SCEs are thus a measure of hyperrecombination leading to chromatid exchange, whether due to deficiencies in genes involved in the suppression of exchange such as the BLM helicase, loss of which leads to the pan cancer-prone Bloom syndrome, or due to unrepaired DNA damage encountered during DNA replication and subsequent HR-mediated repair at stalled replication forks [24–26]. This evidence concerns the gene BLM and Bloom syndrome.