This study is related to a very topical issue at the moment. From a One Health point of view, it is necessary to know the impact that non-antimicrobial molecules can have on the development of resistance, both through mutagenesis and horizontal gene transfer, such as bacterial conjugation phenomena. These results may have implications for the treatment of infections, as well as for the selection of resistance at the environmental level. These data have been published in a journal of high scientific impact, in which an excellent methodological development with the most modern techniques available to address the proposed objectives prevails. 

In recent years, several evidences have shown how non-antimicrobial drugs such as non-steroidal anti-inflammatory drugs, mucolytics such as N-acetylcysteine or even artificial sweeteners such as saccharin can alter bacterial mutagenesis. This work provides new data in this regard. Having this knowledge is important to understand the collateral consequences that these drugs can have on resistance selection. But at the same time, some of these studies have characterised other drugs capable of reducing mutagenesis (this would be the case of some antioxidant treatments used, for example, against Amyotrophic Lateral Sclerosis). Therefore, in these cases, these studies can provide new evidence of the usefulness of known drugs (a priori non-antimicrobial) in the treatment of infectious diseases. 

In the referenced work, a model has been used with laboratory strains in which therapeutic or environmental concentrations of different antidepressants have been used. These results need to be assessed and supported by further trials to understand the consequences in real life. Firstly, it would be necessary to validate whether this behaviour is observed at the same level in clinical isolates of pathogenic species that commonly occur in the clinic; and secondly, whether these phenomena also affect more clinically used antimicrobials such as cephalosporins or carbapenemics (and the resistance mechanisms that affect the activity of these other antimicrobials). Finally, it would be necessary to design patient trials for clinical validation of these findings.