Given that BLA axonal projection is particularly sensitive to Tbr1 haploinsufficiency [17,23] and that BLA activation by local infusion of D-cycloserine, a co-agonist of NMDAR, is sufficient to ameliorate the autism-like behaviors exhibited by Tbr1+/– mice [17], we speculate that BLA-derived circuits are critical to TBR1-linked ASD phenotypes. This evidence concerns the gene TBR1 and autism.