Although humoral immunodeficiencies due to the complete loss of B cell functions (e.g., X-linked agammaglobulinemia or Hyper-IgM syndrome) are unlikely to respond to extrinsic sialylation, conditions in which B cells develop but exhibit sub-optimal function (e.g., Common variable immunodeficiency) may yet be amenable to extrinsic ST6GAL1 therapy (55). This evidence concerns the gene ST6GAL1 and Bruton-type agammaglobulinemia.