The molecular mechanisms that underlie persister cell formation, and antimicrobial tolerance are largely unknown.[1][2] Persister cells are thought to arise spontaneously in a growing microbial population by a stochastic genetic switch,[10][3] although inducible mechanisms of persister cell formation have been described.[10][14] For instance, toxin-antitoxin systems,[15] and a number of different stress responses such as the SOS response,[14] the envelope stress response,[16] and the starvation response have also been associated with persister cell formation in biofilms.[17] Owing to their transient nature and relatively low abundance, it is hard to isolate persister cells in sufficient numbers for experimental characterization, and only a few relevant genes have been identified to date.[2][10] The best-understood persistence factor is the E. coli high persistence gene, commonly abbreviated as hipA.[18]