While XLA, the most severe form of B-cell defects, results from a mutation in the Bruton agammaglobulinemia tyrosine kinase (BTK) gene that causes a B-cell differentiation arrest in the BM, with consequent absence of mature B cells and serum Ig, non-XLA is characterized by hypogammaglobulinemia with decreased B-cell counts in the absence of the BTK gene mutation [47]. This evidence concerns the gene BTK and Bruton-type agammaglobulinemia.