In order to avoid a 5-HT synaptic overload caused by MAOA deficiency, possible counteractions include a stronger SERT gene expression, possibly less controlled by 5HT2BR. Indeed, the SERT gene promoter variants determine different levels of expression affecting 5-HT levels and social skills (Tanaka et al., 2018); a potent clearance of synapses can then be linked with the peripheral hyperserotonemia found in a subset of children with autism, likely carriers of the long allelic variants of the SERT gene promoter (Quinlan et al., 2020). The gene discussed is SLC6A4; the disease is autism.