FOXP2 and childhood apraxia of speech: Mice with certain point mutations in one copy of Foxp2, including those that cause developmental verbal dyspraxia in humans, are developmentally delayed, somatically weak, and have impaired auditory-motor association learning owing to strongly altered activity in the striatal circuits, but they make the expected range of acoustically normal vocalizations (Gaub et al., 2010; French et al., 2012; Kurt et al., 2012).