In summary, in vivo data indicate that while abnormally intensive Fas/FasL interaction can prevent antigen-specific B cell responses (Komano et al., 1999), the defect in Fas function results in uncontrolled autoantibody production, autoimmunity, and increased risk of B cell lymphomas, revealing that the Fas/FasL balance must be very accurately regulated during the humoral immune response. The gene discussed is FASLG; the disease is Autoimmunity.