TP53BP1 and agammaglobulinemia: Given the critical role that RNF168 plays in recruiting 53BP1 to DNA DSBs and the essential requirement for 53BP1 in mediating the repair of DSBs generated during CSR [58,59], it is likely that the antibody deficiency exhibited by the affected patients is directly caused by an inability to recruit 53BP1 to DNA breaks generated within the immunoglobulin locus during antibody diversification.