Several different mechanisms have been suggested to underlie antibiotic persistence, which is the ability of a subpopulation of bacterial cells to tolerate antibiotic treatment without being resistant. Specifically, toxin–antitoxin systems, (p)ppGpp production and ATP depletion have all been linked to persistence, although with contradictory results in different studies and different bacteria. A new study by Pontes and Groisman now finds that Salmonella enterica subsp. enterica serovar Typhimurium can produce persister cells independently of the specific factors listed above and that slow growth alone can explain persistence in their experiments, leading the authors to conclude that there is no dedicated genetic programme that induces persistence, but rather that slowdown of core processes, including those targeted by antibiotics, explains persistence.