The report of Fukuzako et al. describes their results with in vivo 31phosphorus magnetic resonance spectroscopy (31P-MRS) in first-episode, drug-naive patients with schizophrenia. This work follows by 8 years the initial seminal application of phosphorous spectroscopic imaging in this patient population by Pettegrew et al. (9), whose report was notable for identifying abnormalities in phospholipid concentrations in the frontal cortex, potentially implicating pathophysiological processes, both neurodevelopmental and degenerative, and resonating with the enduring phospholipid theories of schizophrenia (10). As interesting as these findings were, the field has been slow to follow them up, perhaps because of the methodological complexities of 31P-MRS (11). In this context, the study of Fukuzako et al. in this issue of the Journal is of considerable interest, particularly because the investigators targeted the temporal lobes, in contrast to previous studies, which acquired spectra from voxels placed in the frontal lobes. Like the previous studies, that of Fukuzako et al. found a decrease of phosphomonoester concentrations and an increase of phosphodiester concentrations. These results suggest that the pathological process responsible for the abnormal phospholipid levels found previously in the frontal cortex is also active in the temporal cortex, which, along with the frontal cortex, is the most strongly implicated anatomical region in the neuropathology of schizophrenia.