“…To further analyze if DC could have selected other mutations, leading to crossresistance to other antibiotics, we measured MICs to antibiotics from other structural families (ceftazidime, imipenem, aztreonam, fosfomycin, tetracycline, and erythromycin) in the populations grown during 4 days in presence of DC, finding no differences respect to the parental strains (Supplementary Table 3). Finally, and although we propose a therapeutic strategy based on a short treatment (3 days; around 20 generations), as we and others have suggested before 28,29,50,74,75 , we analyzed the capacity of DC to select for ciprofloxacin or tobramycin resistance in the long term (15 days; around 100 bacterial generations). We found that this compound did not lead to an increase of ciprofloxacin or tobramycin MICs in the different genetic backgrounds of P. aeruginosa analyzed (Supplementary Table 4) and that, importantly, the capacity of DC to induce transient CS to tobramycin was preserved (Supplementary Table 5).…”