Mutations in the BTK gene in humans cause X-linked agammaglobulinemia (XLA) (Bruton, 1952; Vetrie et al., 1993), which is a primary humoral immunodeficiency characterized by an arrest in the B-cell development, at the transition between the pro-B to the pre-B cell stage, with almost total lack of immunoglobulin production (Campana et al., 1990; Del Pino Molina et al., 2019). This evidence concerns the gene BTK and Bruton-type agammaglobulinemia.