  So, what appears to be the case is that affected KE family members'  language difficulties result from a mutation in the FOXP2 gene, which results in abnormal development of the striatal, cerebellar and  cortical areas necessary for the sequencing and coordination of  speech-related movements of the mouth, tongue and possibly larynx;  MRI scans of affected family members showing reduced gray matter  density in these areas support this hypothesis, as do fMRI scans  showing abnormal striatal and cortical activation during receptive  and active language processing (Belton et al. 2003; Liegeois, et  al. 2003.)