Although previous studies have shown that the levels of CD5+ B cells and IL-10+ B cells are decreased in antineutrophil cytoplasmic antibody-associated vasculitis [38–41] and the frequency of IL-10–producing B cells is higher in hepatitis B virus-associated membranous nephropathy [42], our study is the first to indicate that CD38+CD19+ B cells and Bregs may participate in the pathogenesis of HSPN. The gene discussed is CD38; the disease is anti-neutrophil cytoplasmic antibody-associated vasculitis.