The cause of decreased trogocytosis from PMN to MNC in active SLE remains unclear; however, recent reports demonstrate that epratuzumab (anti-CD22) and a bi-specific hexavalent monoclonal antibody comprising epratuzumab and veltuzumab (a humanized anti-CD20 monoclonal antibody), exhibit enhanced Fc/FcR-dependent trogocytosis from B cells to different immune cells, resulting in a remarkable reduction in B cell surface expression of CD19, CD20, CD21, CD22, and CD79b, as well as the key cell adhesion molecules CD44, CD62L, and β7-integrin [42, 43]. This evidence concerns the gene CD44 and systemic lupus erythematosus.