In the past, GM reduction with MDD was reported, even after remission with antidepressant treatment.2 Regional GM concentration reduction has also been shown to be associated with attentional bias, depressive psychopathology, and cognitive dysfunction.3 MDD has been reported to be associated with WM abnormalities, such as significantly more subcortical WM lesions, in late-onset depression patients.4 In this late-onset MDD patient, increased GM volume and reduced WM volume were observed after amisulpride treatment. Besides, PBVC value also suggested increase of BV. The patient did not have any cerebrovascular disease, which can exclude the possibility of common vascular effects for WM abnormalities in late-onset MDD. Increases of GM volume and BV of this remitted patient also correspond to Phillips et al.’s finding about increased GM volume and BV of remitted MDD patients.5 GM growth effects might be related to reasons such as synaptic remodeling and neurogenesis6 from the stimulation of neutrophic factors by antipsychotics,7 prevention of oxidative stress or 6-OH-dopamine lesioning, and subsequent increased glial cell proliferation in frontal cortex8 and modulation of glutamate receptor function.9 Apart from these possible reasons, amisulpride’s modulating effects of dopamine D2 receptors might help the dopamine system stabilize and modulate neuronal activity through an inverted-U relationship.10 The WM volume decrease in this patient is very interesting. According to reviews of WM volume in MDD, WM should be decreased in MDD because of decreased oligodendrocyte density, reductions in the expression of genes related to oligodendrocyte function, molecular changes in intercellular cell adhesion molecule (ICAM) expression levels, and suggestion of a possible mechanism of ischemia.11 Konopaske et al. found that antipsychotic exposure decreased oligodendrocyte cell number and related myelination of monkeys,12 which might support volumetric decreases of WM in this case.