First described by the paediatrician Ogdon Bruton in 1952, XLA is caused by germline mutations in the Bruton tyrosine kinase (BTK) gene [103] that result in delayed or blocked development of mature B lymphocytes, absent or very low serum immunoglobulin levels and failure of specific antibody production [104]. Here, BTK is linked to Bruton-type agammaglobulinemia.