In schizophrenia, retrospective studies have suggested that head circumference is decreased at birth and developmental delays are present in early childhood, both of which implicate prenatal and early postnatal alterations in forebrain development (Cannon et al., 2002). The occurrence of prodromal symptoms in the majority of cases (Hafner et al., 1994), as well as the presence both prior to and after onset of illness of neuropsychological deficits (Crespo-Facorro et al., 2007) also implicates disruption of forebrain development. Neuropsychological dysfunction implicates the PFC in patients with schizophrenia, the cortical region that has expanded most extensively in mammalian evolution and that has been suggested to rely on key evolutionary developments in stem cell function (Martinez-Cerdeno et al., 2006).