Multidrug tolerant persister cells are not antibiotic resistant mutants. Resistance is caused by newly acquired genetic traits (by mutation or horizontal gene transfer) that are heritable and confer the ability to grow at elevated concentrations of antimicrobial drugs. In contrast, tolerant bacteria have the same MIC (Minimum Inhibitory Concentration) as susceptible bacteria and differ in the duration of the treatment that they can survive. Multidrug tolerance can be caused by a reversible physiological state in a small subpopulation of genetically identical cells, similar to a differentiated cell type. It enables this small subpopulation of microbes to survive the antibiotic killing of their surrounding siblings. Persisting cells resume growth when the antimicrobial agent is removed, and their progeny is sensitive to antimicrobial agents. The molecular mechanisms that underlie persister cell formation and multidrug tolerance are largely unknown. Persister cells are thought to arise spontaneously in a growing microbial population by a stochastic genetic switch, although inducible mechanisms of persister cell formation have been described. For instance, Toxin-Antitoxin (TA) systems and a number of different stresses such as SOS-stress and envelope stress have been associated with persister formation. 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. The best-understood persistence factor is the "E. coli" high persistence gene, commonly abbreviated as "hipA". Although tolerance is widely considered a passive state, there is evidence indicating it can be an energy-dependent process. Persister cells in "E. coli" can transport intracellular accumulations antibiotic using an energy requiring efflux pump called TolC. A persister subpopulation has also been demonstrated in budding yeast "Saccharomyces cerevisiae". Yeast persisters are triggered in a small subset of unperturbed exponentially growing cells by spontaneously occurring DNA damage, which leads to the activation of a general stress response and protection against a range of harsh drug and stress environments. As a result of the DNA damage, yeast persisters are also enriched for random genetic mutations that occurred prior to the stress, and are unrelated to the stress survival   In May 2011, it was reported by Nature.com that the addition of certain metabolites can help suppress multidrug tolerance in numerous species of bacteria, including "E. coli" and "S. aureus", by "the generation of a proton-motive force which facilitates aminoglycoside uptake".