On the molecular and cellular level SIgAD has been associated with a defective terminal differentiation of membrane-bound IgA+ plasma blasts into IgA secreting cells, and this results in defect in the survival of IgA-secreting plasma cells, different T cell abnormalities, an impaired cytokine network, and a defect in the IgA class switching process (121, 134–136). Here, CD79A is linked to selective IgA deficiency disease.