Parvalbumin+ cells have been extensively studied in schizophrenia and evidence of their dysfunction extends well beyond their contribution to the GBO (85, 115, 123). Parvalbumin+ cells have a reduction in mRNA and protein levels of parvalbumin itself despite unaltered neuronal density in patients with schizophrenia observed post-mortem (124–126). Parvalbumin+ cells also have reduced protein and mRNA levels of GAD67 and up to 50% of parvalbumin+ cells are wholly devoid of GAD67 (124). This loss of GAD67 represents a significant decrease in the strength of inhibitory inputs on the pyramidal cells they target (115). Moreover, this deficit has been observed in parvalbumin+ cells across multiple cortical regions including the DLPFC and ACC (127–129). Two hypotheses have been generated to account for the convergent evidence of dysfunction localized to parvalbumin+ basket cells (84). One hypothesis emphasizes the inhibitory contribution to this network interplay and the other excitatory activity. First, lower GAD67 levels in parvalbumin+ basket cells could result in a disinhibition of pyramidal cells. Alternatively, the loss of GAD67 in parvalbumin+ basket cells could be a development disruption due to lack of excitatory input onto these cells to drive their activity. Consistent findings of dendritic spine loss on pyramidal cells in areas like the DLPFC and dysfunction within glutamatergic channels (e.g., NMDA, AMPA) could contribute to this loss of excitatory input onto parvalbumin+ basket cells in schizophrenia (68). These findings support the central importance of parvalbumin+ inhibitory interneurons in schizophrenia pathophysiology but whether this is a primary pathology or homeostatic mechanism in response to diminished pyramidal cell input is still unclear.