This is in line with previous mouse studies showing that maternal microchimerism replaced IL‐2 in IL‐2 deficient offspring,[152] and was a source of IgG‐secreting cells in offspring genetically deficient in B cells.[153] These findings have implications for humans as they may explain why individuals with certain genetic disorders may present a spectrum of disease severity, due to postnatally retained functional maternal microchimeric cells. The gene discussed is IL2; the disease is hereditary disease.