FCGR3A and B-cell chronic lymphocytic leukemia: The above-reported data may suggest that myeloid cells, expanded under the influence of leukemic B cells and acquiring an immunosuppressive phenotype, may directly or indirectly contribute to bone derangement in CLL patients: together with the production of cytokines, such as TGFβ and IL-10, the upregulation of the FcγRIIIa (CD16) antigen also appeared to contribute to the amplification of osteoclasts differentiation.