Along with its well-established role in mitotic progression, the cyclin-dependent kinase CDK2 has recently been shown to be important during gametogenesis – cdk2–/– mice are infertile (although otherwise viable) and spermatocytes in male mice arrest during meiotic prophase I. Little has been known, however, about the details of CDK2's meiotic role. Now, José A. Suja and colleagues (p. 2149) analyse meiotic progression in spermatocytes of cdk2–/– mice, and show that homologous chromosomes pair (synapse) incompletely – notably, however, the synaptonemal complexes and cohesin complexes (both of which connect homologous chromosomes) form normally in these mice. In addition, synapsis occurs extensively between non-homologous chromosomes. The authors next show that, in spermatocytes lacking CDK2, meiosis arrests at a pachytene-like stage (when recombination between homologous chromosomes normally occurs) and chromosomes fail to recombine fully; instead, unrepaired double-strand breaks accumulate. Finally, the authors note that some telomeres do not attach to the nuclear envelope in cdk2–/– spermatocytes, and sex chromosomes fail to form a sex body. Thus, they conclude, CDK2 has a role in ensuring accurate homologous pairing and recombination during mammalian meiosis. These data expand the functional repertoire of CDKs.