Natalizumab treatment was reported to selectively mobilize memory B cells in MS patients which was considered to be secondary to an impaired retention of memory cells in the splenic marginal zone and gut-associated lymphoid tissue (GALT) by blocking very late antigen (VLA)-4/vascular cell adhesion molecule (VCAM)-1 interaction and downregulation of lymphocyte function associated antigen (LFA)-1 and alpha4-beta1 integrin[9]. This evidence concerns the gene VCAM1 and myeloid sarcoma.