The BTBR mouse model is interesting because several ASD‐relevant mRNAs are altered, including Neurexin‐1 and Homer31, which bind30 to Shank1 and Shank3 and has been linked to over activation of the mechanistic target of rapamycin (mTOR) pathway as observed in syndromic forms of ASD such as tuberous sclerosis complex and fragile X syndrome.31 This evidence concerns the gene MTOR and tuberous sclerosis.