Another ITIM-dependent dysregulation of BCR-induced B cell activation in SLE patients might be related to a deficient FcγIIbR mediated suppression; indeed, dysfunction of this low affinity Ab receptor, which is equipped with a cytoplasmic ITIM like LAIR1, is associated with autoimmunity and it has been described in SLE patients [31]. This evidence concerns the gene BCR and systemic lupus erythematosus.