Bacteria can survive “cidal” antibiotic challenge, and this phenotypic tolerance to antibiotics is most notable in cells that are nutrient limited, non-replicating or growing in biofilms. Under such conditions, bacterial stress responses induce protective mechanisms to ensure bacterial survival under stress. My group studies the opportunistic pathogen Pseudomonas aeruginosa and how the stringent response, a conserved starvation and stress response, mediates multidrug tolerance. In particular, regulation of oxidative stress pathways by the stringent response modulates antibiotic lethality, and targeting such pathways may be a novel approach to sensitize tolerant bacteria to conventional antibiotic therapies.