Our data indicate that reduced EV release in FXS neurons is associated with intracellular retention of CYFIP2, suggesting a mechanism for the excess of immature dendritic spines in FXS: when EV-mediated “export” is impaired, CYFIP2 accumulates, potentially dysregulating actin-dependent remodeling and leading to excessive excitatory synapses. This evidence concerns the gene CYFIP2 and fragile X syndrome.