In a Scientific Reports article by Brandhorst et al. it was demonstrated that fludioxonil elicited aldehydic and oxidative stress, and that aldehydic stress could mimic the effects of fludioxonil upon fludioxonil sensitive fungi. As triosephosphate isomerase (TPI) can evolve aldehydic stress in the form of methylglyoxal (MGO), and in vitro evidence showed that fludioxonil lead to an elevation of the release of this MGO, it was postulated that TPI may be a target of fludioxonil. Unfortunately, some have interpreted this article to imply that TPI is the sole direct drug target of this fungicide class. This conclusion is not fully supported by the data, however, as experimental evidence of a direct physical interaction between fludioxonil and TPI in the pathogen has been lacking. Now, further investigation by the Jacob group clearly demonstrates that TPI cannot be the sole direct target of fludioxonil action. We have specifically inactivated the coding sequence of TPI in the genome of the phytopathogenic filamentous ascomycete Magnaporthe oryzae (anamorph: Pyricularia oryzae). We replaced it with a resistance marker gene and proved the successful deletion of the gene. Were the TPI enzyme the sole direct target of the phenylpyrrole fludioxonil, the null mutants ΔMotpi should be resistant to fludioxonil compared to the wildtype strain upon phenylpyrrole treatment. This is not the case.