The long repeat of the CGG sequence prevents the expression of the encoded FMRP protein, which leads to alterations in the development of synapses, including thin and elongated dendritic spines with increased density, and immature synaptic connections, as evidenced by studies with FXS animal models and postmortem studies of FXS individuals (Rudelli et al., 1985; Hinton et al., 1991; Comery et al., 1997; Irwin et al., 2002). The gene discussed is FMR1; the disease is fragile X syndrome.