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In clonal bacterial cultures, where all cells are genetically identical, individual bacteria can nevertheless express different traits, giving rise to a diverse and complex population of phenotypic variants. This phenotypic heterogeneity allows single organisms to survive in conditions that are lethal for most of the population, such as assault with antibiotics (1). The survivors can then live on and regenerate the population when conditions become favorable again. To prevent this type of antibiotic failure, a greater understanding of the mechanisms that underlie phenotypic heterogeneity is essential. On page 311 of this issue, Bergmiller et al. (2) uncover such a mechanism.