In Fc gamma receptor IIb- (Fcgr2b-) deficient mice that develop fatal lupus pathology, IL-17A/Act1 signaling has been shown to adversely affect the course of glomerulonephritis by promoting the recruitment of immune cells in particular neutrophils and NET deposition in inflamed kidneys [79]. The gene discussed is IL17A; the disease is systemic lupus erythematosus.