On the basis of EVB methodology, we accurately investigatedthe catalytic performance of MAO enzymes, focusing on the effectsof artificially designed MAO-A and MAO-B point mutations (i.e., mutantswithout known neuropsychiatric impact)23−25 and substrate selectivity.26−28 In addition to that, we addressed two MAO-A mutants known to beassociated with the Brunner syndrome, namely, R45W and E446K, andfound a significant slowdown of serotonin degradation29 compared to the WT enzyme, which is in agreement with theclinical picture of the patients carrying these mutations. The gene discussed is MAOA; the disease is Monoamine oxidase A deficiency.