Vav1 is a guanine nucleotide exchange factor essential in the development and function of alphabeta lineage T cells. Here we report that in contrast to profound effects on pre-TCR- or alphabeta TCR-dependent events in thymocyte development, Vav1 deficiency has no detectable effect on the development of gammadelta T cells. Strikingly, however, these gammadelta T cells are markedly deficient in signaling through the gammadelta TCR, as evidenced by a lack of proliferation and cytokine production in response to stimulation with anti-gammadelta TCR antibodies. We propose that Vav1 has a unique and non-redundant role in the initiation of signaling downstream of the gammadelta TCR in lymphocytes.