Pyk-2, also known as RAFTK, is a tyrosine kinase closely related to focal adhesion kinase (FAK), and is activated by many different stimuli, including signaling by chemokine and lipid receptors, integrins, antigen receptors and ion channels6. Expression of Pyk-2 is widespread, although one splice variant is somewhat restricted to hematopoietic cells6. The types of signals leading to Pyk-2 activation and its similarity to FAK have suggested a role in integrating signals that control cell adhesion and motility. To characterize the role of Pyk-2 in vivo, Okigaki and Schlessinger inactivated the

Pyk2 gene in mice. During analysis of these animals, Guinamard and colleagues made the discovery that they lack splenic marginal zone B cells1. Testing for effects of this deficiency on antibody production, Pyk-2–/–mice exhibited a deficit in IgG3 responses to the multivalent polysaccharide Ficoll, a T-independent type II antigen. IgM and IgG2a production were also diminished. T-dependent responses were less affected although there was a slight reduction in IgM production. An important role for marginal zone B cells in T-independent antibody responses is therefore strongly supported by this study.