This targeting approach is supported by studies from our lab and others that have reported a caspase-independent role for XIAP in mediating survival signaling and ROS suppression, in particular, through activation of NF-κB and its target genes (for example, antioxidant enzymes SOD1 and SOD2 among others).17, 33, 42 These data support this additional mechanism of XIAP in modulating redox response in cancer cells and this study is the first to observe that XIAP can abrogate ADCC-mediated cell death in a caspase-independent manner. Here, SOD1 is linked to cancer.