PVALB and schizophrenia: Based on the NMDA receptor hypofunction hypothesis of schizophrenia [75, 76], cerebello-thalamo-cortical hyperconnectivity is supposed to result from NMDA receptor deficits impeding the functioning of cortical parvalbumin-containing gamma-aminobutyric acid (GABA) interneurons which fail to inhibit pyramidal glutamatergic neurons eliciting upregulated FC within this circuitry [73, 77].