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The Anthrax toxin receptor (ATR) was initially discovered as the tumor endothelial marker 8 (TEM8).1 This protein, which exists in three isoforms (36, 40, and 60 kDa), is highly expressed in tumor vessels as well as in the vasculature of developing embryos, suggesting that it may normally play a role in angiogenesis. However, it also acts as the receptor for anthrax toxin.2 Following the binding of this protein by the protective antigen (PA) of anthrax, PA is cleaved and heptamerizes to form the binding site for both edema factor (EF) and lethal factor (LF).3 This complex is then endocytosed by the cell; acidification in endosomes allows the release of EF and LF into the cytoplasm where they interfere with MAPK signaling and induce apoptosis.4