The incidence of rapid debrisoquine metabolizers is higher in BEN patients than in healthy controls [9]. CYP2D6 polymorphic variants predisposing to toxic effect of various chemical agents are suspected in BEN pathogenesis. LCAT-deficient individuals have evidence of renaltubular injury and this defect can be involved in BEN [10]. The gene discussed is CYP2D6; the disease is Balkan nephropathy.