In conclusion, our study further supports the notion that heterozygous alterations of TNFRSF13B/TACI alone do not result in overt CVID but may be also found more frequently in distinct clinical phenotypes, including IgG subclass deficiencies, benign lymphoproliferation and, as recently shown, autoimmunity [19] and Good's syndrome [20]. Here, TNFRSF13B is linked to common variable immunodeficiency.