By taking in mind that mTOR is activated in response to insulin while hyperactive (aberrant) mTOR promotes IRS1 inhibition (Copps and White, 2012), observations collected with regard to the use of rapamycin spurs the necessity to better understand whether hyperactivation of mTOR results from the dysfunction of the insulin signaling pathway or is a primary cause of the observed impairment of the pathway in DS. This evidence concerns the gene MTOR and Dravet syndrome.