It is also possible that the lack of efficacy of mTOR inhibitors observed in some studies of tuberous sclerosis was due to the specific inhibition of the mTOR1 path, leaving mTOR2 functional; or because of the simultaneous alteration in the mTOR path with others such as Atg7 [79]; or simply because the functional alterations seen in ASD are of different intrinsic or extrinsic causalities (metabolic, inflammatory, etc.)and neuronal apoptosis is not always mTOR-driven. This evidence concerns the gene ATG7 and tuberous sclerosis.