The role of CD16 is further supported by the observation that the clinical response to therapeutic mAb treatments is affected by a single nucleotide polymorphism (SNP) of the FCGR3A gene that affects binding affinity for IgG; indeed, patients that are homozygous for high-affinity allelic variant (FcγRIIIA-158-V/V) display better clinical outcome to therapeutic mAb regimens than those heterozygous (FcγRIIIA-158-V/F), or homozygous for low-affinity variant (FcγRIIIA-158-F/F), in follicular (FL) and non-Hodgkin’s lymphomas, CRC, and breast cancer [84,85,86,87,88]. This evidence concerns the gene FCGR3A and breast carcinoma.