Specifically, increased synthesis of galactose-deficient IgA1 as the first hit, production of antiglycan IgG and/or IgA1 autoantibodies as the second hit, and poorly galactosylated IgA1 and antiglycan IgG autoantibodies form immune complexes and deposit in the mesangial area of the glomerulus from the subsequent hits [111] The deposition of IgA1 immune complexes causes mesangial cell, podocyte, and tubular epithelial cell damage, leading to end-stage renal disease in patients with IgAN. The gene discussed is IGHA1; the disease is stage 5 chronic kidney disease.