In our view, the failure of beneficial antidepressant treatment to affect [11C]harmine binding as measured by PET dissociates depressive psychopathology from central levels of monoamine oxidase type A. The relationship reported between elevated activity of monoamine oxidase type A in some brain regions and recurrence of depression was statistically significant without correction for multiple comparisons, but inspection of the data indicates marked overlap between groups, which tends to call that finding into question. The gene discussed is MAOA; the disease is depressive disorder.