Chromosome breakage — a dangerous event that has triggered the evolution of several double-strand break repair pathways — has been co-opted by the immune system as an integral part of B- and T-cell development. This is a daring strategy, as improper repair can be deadly for the cell, if not for the whole organism. Even more daring, however, is the choice of a promiscuous transposase as the nuclease responsible for chromosome breakage, as the possibility of transposition brings an entirely new set of risks. What mechanisms constrain the dangerous potential of the recombinase and preserve genomic integrity during immune-system development?