We note that existing data already suggest that genetic robustness is relevant to the evolution of antibiotic resistance in bacteria. Research shows that compensatory mutation is an important underlying genetic mechanism for maintenance of resistance in the absence of antibiotic selection. 53 This epistasis mechanism explains how a resistance gene that is costly for bacterial growth in absence of an antibiotic may be compensated by one or more mutations in the plasmid or bacterial chromosome, effectively eliminating the cost of carrying the resistance gene ͑or the plasmid on which it re-sides͒ when no antibiotic is present. If a bacterial strain contains a compensatory mutation that interacts to reduce the cost of various different resistance genes, then this epistatic mutation would provide an example of a genetic-robustness allele responsible for environmental robustness across antibiotic environments. For example, the multiple antibiotic resistance locus in E. coli and several species of Salmonella is involved with production of an efflux pump that removes various antibiotics from the cell, affording low-level clinical resistance. 54 However, this mode of resistance can be rather costly if transport in and out of the cell is not tightly regulated. Evidence suggests that the low-level resistance may be a stepping-stone to more finely tuned evolved mechanisms allowing greater resistance, 55 and we can conceive that genetic changes simultaneously compensating to reduce the cost while maintaining the broad resistance would provide an example of a genetic-robustness allele.