The bacterium Pseudomonas aeruginosa copes with a trade-off between mucosal colonization and antibiotic tolerance in respiratory tract infections.[1] Biofilm formation, which protects against antibiotics, creates a metabolic burden because the production of a sticky matrix consumes resources and slows the spread of the bacterium.[1] In the planktonic state, the bacterium spreads better and obtains nutrients, but is more vulnerable to antibiotics.[1] Using the Tn-seq technique, scientists have identified genes important for survival in mucosal colonization and antibiotic tolerance.[1] Computer modeling has revealed the exact metabolic pathways that the bacterium relies on in the lung environment.[1] The study highlights the need for infection models mimicking the physiology of human tissues to combat antibiotic resistance.[1]