Moreover, deficits in high-frequency oscillations highlight the contribution of specific GABAergic interneurons, such as parvalbumin or somatostatin-expressing interneurons13,57 that are impaired in visual areas in schizophrenia.58 In addition to the pharmacologic correction of aberrant circuit dynamics, it is also conceivable that interventions that improve the fidelity of sensory processing through cognitive remediation59 or brain stimulation60 could potentially prevent the progression of circuit dysfunctions from sensory areas to more extended networks. The gene discussed is PVALB; the disease is schizophrenia.