In initial studies, we showed that anthrax toxins act on Drosophila homologs of their known targets in mammalian cells (Guichard et al., 2006) . In addition to these known effects of LF and EF, we observed that both toxins also caused adult wing and bristle phenotypes similar to those caused by inhibition of the Notch signaling pathway, and blocked expression of Notch target genes in developing wing imaginal discs (Guichard et al., 2010) . Moreover, these toxins interacted in a synergistic fashion to block Notch signaling (Fig. 3A) . Further analysis of this Notch-like phenotype revealed that it resulted from failure to recycle the Notch ligand Delta to the cell surface (Guichard et al., 2010) . EF was found to reduce the levels and activity of the small GTPase Rab11, whereas LF reduced cell surface levels of the Rab11 binding partner, Sec15 (Fig. 3B ). Sec15 is part of an octameric protein complex known as the exocyst, which targets proteins, including Delta and the cell adhesion molecule DEcadherin, to adherens junctions (accordingly, DE-cadherin trafficking to adherens junctions was also reduced by EF and LF). These results from flies were validated in human vascular and lung endothelial cells by our collaborators in Victor Nizet's laboratory (Fig. 3C) , who also showed that EF reduced epithelial barrier integrity in a cell culture assay and in vivo in mice (Guichard et al., 2010) .