Aitman et al. showed that  copy number variation of the orthologous rat and human Fcgr3  genes is a determinant of susceptibility to immunologically mediated glomerulonephritis. Positional cloning identified loss of the rat-specific Fcgr3 paralog 'Fcgr3-related sequence' (Fcgr3rs) as a determinant of macrophage overactivity and glomerulonephritis in Wistar Kyoto rats. In humans, low copy number of FCGR3B, an ortholog of rat Fcgr3, was associated with glomerulonephritis in the autoimmune disorder systemic lupus erythematosus (SLE. Aitman et al.  concluded that their finding that gene copy number polymorphism predisposes to immunologically mediated renal disease in 2 mammalian species provides direct evidence for the importance of genome plasticity in the evolution of genetically complex phenotypes, including susceptibility to common human disease.