The accumulated evidence shows that the possible mechanism of ART in treating IgA nephropathy includes two aspects: ARS can inhibit the production of inflammatory cytokines (such as IL-6 and TGF-β) and block the overactivation of B lymphocytes [37], inhibit the synthesis of Gd-IgA1, and reduce the production of IgG and/or IgA1 autoantibodies, reducing the severity of IgA nephropathy. Here, TGFB1 is linked to IgA glomerulonephritis.