Consistent with the above-described role of Lyn in maintaining ITAMi-mediated immune homeostasis, i.p. administration of the NTN serum led to a severe acute nephritis associated with high mortality at day 7 in Lyn-deficient FcγRIIATg recipients, whereas mice deficient for Lyn or Fyn and Fyn-deficient FcγRIIATg mice did not develop significant disease despite similar glomerular rabbit antibody deposits and no significant differences in mouse IgG anti-rabbit IgG responses (Fig. 4a and Supplementary Fig. 6a). The gene discussed is FYN; the disease is nephritis.