In addition to the diminished expression of CD3ζ, it was shown that the functionally and structurally homologous Fc receptor gamma subunit (FcRγ) occupies the binding space of CD3ζ which may play a major role in the aberration of the antigen receptor-initiated signaling and therefore lead to a variety of pathogenic changes in the SLE T cell phenotype (46, 50). This evidence concerns the gene FCER1G and systemic lupus erythematosus.