These findings suggest that LAT1 is critical for the maintenance of normal brain BCAA levels.[13] This study also showed that LAT1 loss of function leads to autism spectrum disorders and motor dysfunctions in humans and mice and that intracerebroventricular administration of BCAA ameliorates abnormal behaviors in mice.[13] Furthermore, the deletion of LAT1 in neural progenitor cells affects the postnatal metabolic state, neuronal survival, and persistent behavioral defects.[14]. Here, SLC7A5 is linked to autism spectrum disorder.