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Pathogenic E coli including enteropathogenic E. coli (EPEC) contaminate water and food supplies and causes infantile diarrhea. In developing nations EPEC causes sickness in some 20 million per year, killing ~500,000. EPEC form actin-filled membrane protrusions or bedestalsb(also called attaching and effacing (A/E) lesions) beneath themselves on the surface of intestinal epithelial cells. In the cover image, actin pedestals (green) are seen extending from the cell beneath attached bacterium (small blue dots). Pedestals permit colonization of the host, and are required for subsequent development of disease. The watershed event in EPEC pathogenesis and pedestal formation is the phosphorylation of the EPEC virulence factor Tir by a host cell tyrosine kinase, which permits recruitment of Nck, N-WASP, and the Arp2/3 complex, and subsequently actin polymerization. We have shown (see Swimm et al. MBC 15; 3520-3529) that kinases of the Abl family are recruited and activated beneath attached bacteria. The localization of Abl kinase (in red) is shown apposed to the attached EPEC and colocalized with the actin. We show that Abl-family kinases are sufficient for catalyzing Tir phosphorylation and actin pedestal formation, and we suggest that, rather than using a particular kinase, the pathogen can use any of several redundant kinases, perhaps to expand the repertoire of infectable cell types. —Alyson Swimm and Daniel Kalman