To explain the mechanisms of this resistance, different alterations in host immunologic factors have been assumed, such as (i) CDC unresponsiveness due to altered expression of CD46, CD55, and CD59 (complement-regulatory proteins) on tumor cells; (ii) ADCC resistance due to changes in the lipid raft and FcγRIIIa polymorphisms, causing failed recognition of the CD20/antibody complex by effector cells; (iii) selection of apoptosis resistant clones as a consequence of repeated exposure to Rituximab; and (iv) selection of CD20− tumor clones [27,28]. This evidence concerns the gene FCGR3A and neoplasm.