Some simple ones are easily justified. Pathogens should be screened whenever possible to ensure that antibiotics are targeted against sensitive bacteria. Research should be supported to discover new antibiotics more rapidly than pathogens are able to evolve resistance. However, given the slow pace of drug development, there has also been the desire to consider more complex strategies that stop, or minimally, slow the evolution of resistance. For example, is the coordinated use of two drugs better than random administration? Antibiotics have been cycled and argued to be an improvement over the status quo. Switching from cephalosporin to carbapenem over a period of one year increased the frequency of resistance to carbapenem in a hospital while the level of cephalosporin resistance was reduced. Long-term antibiotic switching deployments are necessary to determine whether resistance reductions are sustainable. Multi-drug EX 527 cocktails have been deployed with success against cancer, HIV, tuberculosis and agricultural pathogens. However, the mechanisms responsible for these successes and their long-term consequences are not well understood. Are multi-drug cocktails effective because they are analogous to a two-front offensive on a pathogen? Can patients be effectively treated with low-dose multi-drug cocktails? Are multi-drug cocktails capable of a sustained reduction in the frequency or level of antibiotic resistance? Confounding these issues is the perception that the use of antibiotics necessarily introduces a tragedy of the commons dilemma. While an individual is helped by antibiotic treatment, the future public is hurt because the treatment naturally selects for the evolution of more prevalent and increased resistance in the environment. Limiting antibiotic use can control the evolution of resistance, but how such a policy translates to improved health outcomes remains unclear. The ultimate goal of sustainable management of limiting antibiotic resources should be the treatment and healthful recovery of the patient, not necessarily a reduction in prevalence of antibiotic resistance. Otherwise, the optimal strategy for antibiotic use is trivial: a global ban. Increased microbial sensitivity to chemotherapeutic agents when used in combination, rather than in isolation, was first documented by a seminal study that sought to classify antibiotics by measuring cross-resistance. Further inquiry showed that the minimum drug concentration required to inhibit microbial growth can be reduced in multiple clinically-isolated drug-resistant pathogens with the addition of sodium clavulanate. Indeed, in some cases minimum inhibitory concentrations of clinically relevant pathogens decreased by four orders of magnitude. These early studies show that the evolution of antibiotic resistance can be managed, but not reversed. However, later research focused illustrates that the combination of tetracycline and fusaric acid can selectively enrich tetracycline-sensitive mutants from clonal populations of tetracycline-resistant bacteria. Mechanistically, this occurs because the efflux pump responsible for tetracycline resistance is hindered in the presence of fusaric acid. These studies serve as a proof-of-concept that resistance characters harbored by human pathogens can be controlled in the lab.