Enteric pathogens finely regulate the expression of virulence genes in response to stimuli generated by the intestinal environment. Diarrheagenic Escherichia coli together, have emerged as probably the most important enteric pathogens for man. E. coli and Salmonella spp. have a great propensity from harmless commensals to change into opportunistic and/or specialized pathogens that possess specific virulence attributes promoting the ability of the organism to cause disease. E. coli pathotypes, Klebsiella spp. and Salmonella spp. developed strategies to cause intestinal secretion through the elaboration of factors that share structure and function with specific host counterparts. EAST1 toxin may subvert multiple cellular processes to yield intestinal epithelial cell secretion and is an example of enteric toxin that activates the transcellular secretion pathway by mimicking guanylin, the endogenous modulator of cGMP signalling. Salmonella developed one strategy to induce intestinal secretion through the elaboration of a factor (SopB) that resembles at least two of the host cell 4-phosphatases, enzymes that activate the Ca⁺-depend transcelullar secretion pathway. EAST1 is a small protein encoded by astA gene that was observed in all diarrheagenic E. coli categories, in E. coli without known virulence genes, in some Salmonella spp. and in Klebsiella pneumoniae strains isolated from patients with chronic diarrhea. There are several hypotheses on how astA was transferred in these strains, as well as the role of this toxin in causing sporadic diarrheal illness and its associations with other genes lying in the proximity of astA as virulence determinants such as toxins and/or adherence factors.