CD3γ-deficient mice have a severe block in T-cell development (7), whereas the loss of the CD3γ protein in humans has been shown to allow the development of polyclonal T cells, maintain TCR/CD3 signaling, and be associated with a less severe phenotype, characterized by a varying degree of susceptibility to infection and the frequent occurrence of autoimmune disorders (8–10). This evidence concerns the gene CD3G and infection.