Abstract
Recent observations of frequent recombinase-mediated interchromosomal exchanges between separate antigen receptor genes in normal lymphocyte precursors have provided clear examples of the ability of the recombinase to catalyze chromosomal translocation events, some of which may actually contribute to increased diversity of antigen receptor proteins. These findings have established that, even in the normal setting, the recombinase is not constrained to act only on gene segments linked in cis, but can also function in trans. Certain tumor-associated chromosomal translocations can be explained as subversions of this enzymatic capability.