These treatments either deplete B cells (anti-CD20, anti-CD52, anti-CD74, anti CD19, anti-CD22) and plasma cells (anti-CD38) or inhibit B cell survival (anti-B-cell activating factor [BAFF]), impair activation (proteasome inhibitors, tyrosine kinase inhibitors) or interaction with T cells (anti-CD80/86) (2) and all have the potential to cause iatrogenic secondary antibody deficiency. Here, TNFSF13B is linked to agammaglobulinemia.