In this context, in vitro mechanism-of-action studies have shown that epratuzumab binding to CD22 on B cells leads to rapid internalization of the antibody–CD22 complex [3], phosphorylation of immunoreceptor tyrosine–based inhibitory motifs on the CD22 intracellular tail [3], diminished proliferation of isolated B cells from patients with SLE [4], and modification of migration of B cells [5]. This evidence concerns the gene CD22 and systemic lupus erythematosus.