Using a humanized model of treatment refractory B cell leukemia, and the CD52-specific antibody alemtuzumab, Pallasch et al. found that FcγRIIB is highly overexpressed on leukemic tumor cells in such antibody drug-resistant tumor microenvironments, and that shRNA-mediated knock-down of tumor cell FcγRIIB restored responsiveness to therapeutic antibody resulting in animal cure (70). This evidence concerns the gene FCGR2B and neoplasm.