Schizophrenia is a complex disorder known for its positive symptoms: delusions and hallucinations. However, the impact of schizophrenia on function is mostly due to its executive dysfunction. Mechanistically, it is known that the prefrontal cortex (PFC) is dysfunctional in this disorder and that there is a general excitatory/inhibitory (E/I) imbalance in the schizophrenia brain. However, whether schizophrenia executive dysfunction can be specifically attributed to prefrontal E/I imbalance is unknown. Here, through a series of experiments across schizophrenia-relevant mouse models, we show the mechanistic plausibility of this hypothesis. First, we show that a critical molecular regulator of synaptic inhibition is reduced across several schizophrenia-relevant models, and in at least one of them, this is PFC specific. Second, we show that this leads to reduced synaptic inhibition in principal cells of the PFC in acute slices. Third, we show that this translates to reduced signal-to-noise ratio of prefrontal neural responses to optogenetic stimuli, which are accompanied by deficits in two prefrontal dependent behaviors; working memory maintenance and task switching. A PFC-selective genetic manipulation of removing this molecular regulator reproduces these phenotypes and a systemic pharmacological approach to augmenting it rescues network and behavioral deficits in disease model animals. Altogether, our work shows a direct link between prefrontal E/I balance and executive dysfunction in schizophrenia with multiple future avenues involving neural modeling and clinical translation.