Loss of FMRP and subsequent overabundance of neuronal proteins in the brains of patients and mouse models of FXS induces a complex and debilitating neurological phenotype, including impaired cognition and social interactions, hyperactivity, attentional deficits, seizures, hypersensitivity, autistic behaviors, and autonomic dysfunction [1, 2, 13–17]. The gene discussed is FMR1; the disease is fragile X syndrome.