The FccRIIIA receptor (CD16A) is the dominant FccR involved in human NK cell-mediated ADCC. Treatment of CCR4 + Mac-1 tumor bearing mice with AAV8-h1567 and human PBMCs resulted in a marked increase in the number of tumorinfiltrating human CD56 + NK cells, suggesting that CD16A which is expressed on human NK cells is involved in this tumor cell killing through it's interaction with the Fc portion of h1567, a finding that has been experimentally confirmed through Fc mutagenesis studies (data not shown). Moreover, in vitro ADCC studies with purified human NK cells demonstrated a concentration dependent killing by h1567 (Figure 4c) . Thus the unifying observations from both treatment studies strongly suggest that the in vivo anti-tumor activity of h1567 is mediated, at least in large part, by ADCC through engagement of FccRIIIA on mouse neutrophils (model 1) and human NK cells (model 2). Since Fc gamma receptors (FccRs) of different types are present on a variety of effector cell populations, including NK cells, dendritic cells, macrophages, monocytes and neutrophils [33, 34] , it is possible that FccR engagement on other immune effector cells, not investigated in this study could also be involved.