Nevertheless, it is unknown whether anomalies in MAP-Tau actively contribute to the pathology of these diseases, as was originally proposed by Tai and collaborators (in which 50% in Tau reduction was sufficient to prevent or diminish autism-like behaviour in animal models of ASD), or whether they are rather the result of the neurotoxic effects of mTOR overstimulation [67,68]. The gene discussed is MAPT; the disease is autism.