Background: Schizophrenia (SCZ) is frequently associated with marked working memory (WM) deficits whose pathophysiology is closely related to dorsolateral prefrontal cortex (DLPFC)-dependent dysfunction[1]. These deficits predict disease outcome and poor response to antipsychotic treatment[2]. Consequently, elucidating the physiology of DLPFC-dependent WM deficits in SCZ is key in better understanding this illness and its treatment.