They based their supposition on findings that U-CLL cells express higher proportion of mannosylated surface μ chains compared to M-CLL, that the high-mannose glycoform is reverted in vitro to the mature complex form, and that μ chains of normal B cells convert their glycan type from a complex to a high-mannose form in response to continuous ligation of surface IgM by anti-μ heavy chain antibodies. This evidence concerns the gene CD40LG and B-cell chronic lymphocytic leukemia.