We therefore tested the hypothesis that abnormally high levels of FOXG1 and its downstream genes could be responsible for the phenotypic abnormalities identified in neuronal cells of macrocephalic ASD patients. To this end, using lentiviruses carrying short hairpin RNAs (shRNAs) targeting FOXG1, we tested whether an attenuation of the FOXG1 expression level in patients’ neural cells was able to revert some of the neurobiological alterations.
