In humans, the strongest evidence for a role of FcγR-mediated effector function in tumor-targeting antibody-based cancer therapies (e.g., rituximab) derives from studies demonstrating an association between clinical responses and specific alloforms of activating FcγRs conferring higher binding affinity to IgG1 or IgG2, particularly the CD16a-V158F and CD32a-H131R SNPs, respectively (Cartron et al., 2002, Musolino et al., 2008, Weng and Levy, 2003, Zhang et al., 2007). Here, FCGR3A is linked to neoplasm.