Simultaneously, these interventions modulate TGF-β1/Smad family member 3 (Smad3) signaling to reduce immune complex deposition in IgA nephropathy (IgAN) and mesangial proliferative glomerulonephritis (MsPGN) (Pei and Li, 2021; Wu et al., 2024), while enhancing erythrocyte-mediated clearance via redistribution of circulating complexes to erythrocyte surfaces—a mechanism shown to limit renal deposition (Hu et al., 2011). The gene discussed is SMAD3; the disease is IgA glomerulonephritis.