Wiskott-Aldrich syndrome (WAS), characterised by recurrent infections and abnormal lymphocyte function is commonly caused by loss-of-function mutations in WAS protein (WASp) or in its interacting protein WIP (Lanzi et al., 2012; Thrasher and Burns, 2010), both of which are involved in triggering actin polymerisation downstream of Cdc42 (Martinez-Quiles et al., 2001; Moreau et al., 2000). The gene discussed is WAS; the disease is Wiskott-Aldrich syndrome.