These spines’ morphological defects on DAP-treated DCX+ cells are reminiscent of those observed on mature neurons from mutant mice of the fragile X mental retardation protein (Fmr1) (Braun & Segal, 2000) and from human patients’ brains that suffer from the fragile X syndrome (Irwin et al, 2000). The gene discussed is DCX; the disease is fragile X syndrome.