In SIgAD, although the underlying pathogenetic mechanism is not yet fully elucidated, the reduction of serum and secretory IgA can lead to colonization and penetration by pathogenic bacteria, and facilitate the passage of aeroallergens and food antigens, predisposing patients with SIgAD to a higher risk of developing allergies. This evidence concerns the gene CD79A and selective IgA deficiency disease.