In experimental anti‐MPO glomerulonephritis, anti‐CD25 mAb Treg depletion enhanced anti‐MPO‐specific autoimmunity and exacerbated disease.25 Mechanisms that enhance Treg number and function, including IL‐10‐secreting mast cells,26 and nasal insufflation of an immunodominant CD4+ T‐cell MPO epitope, MPO409‐428, protect mice from experimental anti‐MPO autoimmunity and glomerulonephritis.27 Therefore, observational and experimental data in AAV suggest that strategies that enhance Treg function may lead to more targeted therapies. This evidence concerns the gene IL10 and glomerulonephritis.