From a mechanistic standpoint, these results move the field beyond well-established paradigms in the autism literature, such as the imbalance between glutamate and GABA to explain insistence on sameness and the co-morbidity with epilepsy [62], or the role of 5-HT in reference to hyperserotonemia, disruption of circadian rhythmicity, neuroinflammation and neuronal excitability [63,64,65]. The gene discussed is HTR5A; the disease is autism.