While WAS−/− mice, in contrast to WAS patients, have normal levels and production of antibodies, WAS−/− mice show similarities to WAS patients too: e.g. defects in T-cell receptor–induced proliferation and aberrant regulation of the actin cytoskeleton, as well as reduced numbers of Tregs, resulting in lymphopenia [86]. The gene discussed is WAS; the disease is Wiskott-Aldrich syndrome.