Beyond providing a multicellular model for assigning known biochemical activities to virulence factors, Drosophila can also be used as a tool to discover completely new activities of virulence factors. For example, Bacillus anthracis, the etiological agent of anthrax, produces two toxic factors required for systemic virulence (Lacy and Stevens, 1999; Mourez, 2004; Tournier et al., 2007; Guichard et al., 2011) : lethal factor (LF), a zinc metalloprotease that cleaves MAPKKs (Duesbery et al., 1998; Vitale et al., 1998) , and edema factor (EF), a highly active calmodulin-dependent adenylate cyclase (Leppla, 1982) . Both LF and EF are essential for the lethal effects of anthrax (Pezard et al., 1991) , which culminates in vascular failure and septic-shock-like death. An important unanswered question is, how do LF and EF, with such seemingly disparate enzymatic activities, collaborate during infection (particularly within vascular endothelial cells, which become leaky at advanced stages of disease, leading to death)?