In SIgAD, although the underlying pathogenetic mechanism is not yet fully elucidated, the reduction of serum and secretory IgA may lead to colonization and penetration by pathogenic bacteria and also promote the passage of aeroallergens and food antigens, making SIgAD patients more prone to recurrent infections, autoimmunity, and allergies [10,11]. This evidence concerns the gene CD79A and selective IgA deficiency disease.