Heart rhythm and conduction disorders are a serious problem in chronic psychopharmacotherapy of schizophrenia. One potentially fatal antipsychotic-induced adverse reaction is drug[1]induced long QT syndrome, which is a phenomenon of prolongation of cardiac repolarization and leads to an increased risk of ventricular tachycardia, known as Torsades de pointes, in the presence of an administered drug [1]. The clinical diagnosis of this adverse drug reaction is difficult, however, electrocardiography and Holter ECG monitoring are the gold standard for the functional diagnosis of long QT syndrome, although they do not give the psychiatrist an answer about the possible correction of mono- or polytherapy for schizophrenia in a particular patient. Pharmacogenetic testing is an integral part of the personalized strategy of psychopharmacotherapy in modern psychiatry. Slowing the efflux of antipsychotics through the histohematic barriers and the membrane of neurons and cardiomyocytes, along with slowing down the metabolism of antipsychotics in the liver with the participation of cytochrome P450 enzymes, can significantly increase the risk of antipsychotics induced long QT syndrome and sudden death syndrome. The purpose of this clinical case is to update the existing problem of pharmacogenetic testing in real psychiatric practice and demonstrate possible ways to solve the problem of antipsychotic-induced long QT syndrome in a young man with paranoid schizophrenia.