However, FcγR affinity-reducing polymorphisms and several immunomodulatory mechanisms in the tumor microenvironment (TME) including alternatively-activated immune effector cells, and expression of inhibitory Fcγ receptors, may limit the ability of IgG1 antibodies to effectively stimulate immune responses within tumor lesions.7, 10 IgE class mAbs may offer an alternative approach to activate the immune microenvironment. Here, FCGR2A is linked to neoplasm.