Regarding the enhanced surface expression of FcμR on CLL B cells, CLL-derived BCRs, unlike those from other B cell malignancies, have been shown to ligate each other via interactions between Ig HC CDR3 of one BCR and the framework region 2 of another BCR irrespective of their IGHV mutation status, thereby providing antigen-independent cell-autonomous signaling (90, 91). This evidence concerns the gene FCMR and B-cell chronic lymphocytic leukemia.