  The failure of FOXP2 to perform its normal role in turn leads to abnormal brain development in affected KE individuals. Studies of other animals and humans (e.g., Lai et al. 2003; Takahashi et al., 2003; Ferland et al. 2003; Teramitsu et al. 2004) show that FOXP2 is normally highly expressed in both development and adulthood in two distinct brain circuits, One is a corticostriatal circuit, in which inputs from the prefrontal and premotor cortex are modulated by the basal ganglia and the thalamus, and then sent back to prefrontal and premotor cotical areas; the other is an olivocerebellar circuit, in which sensory input is sent via the spinal cord for processing in the medulla, cerebellum and thalamus before being handed on to prefrontal cortex. (See fig. 7.) The basal ganglia are known to be involved in the sequencing and reward-based learning of motor behaviors (Graybiel 1995, 1998), and the cerebellar circuit, while less well understood, is thought to be a proprioceptive circuit involved in motor regulation and coordination (Lieberman 2002). FOXP2 is expressed in homologues of these areas in other species (e.g., canaries, zebra finches, rats) and in all species studied, these areas are involved in motor sequencing and coordination (Sharff and White 2004).