As we known, the infections activate the mucosal immune system, which has been recognized to contribute to the onset of IgAN, causing it to produce excess IgA, leading to the deposition [1, 2, 13]. In the renal specimens of IgAN patients, the antigens of Human Cytomegalovirus, Adeno and Herpes simplex virus, Epstein-Barr virus, and even Staphylococcus have been detected, accompanied by the IgA deposits [13, 14]. The gene discussed is CD79A; the disease is infection.