Indeed, several targets we identify as reduced in translation have been implicated in FX (i.e., Hcn2, Shank1, Pde2a) or autism (i.e., Cdh2, Cacna1c, Gabra5)81–84, and are consistent with the reductions in calcium channel function, GABA receptor activity and dendritic spine maturity that are seen in the Fmr1−/y mouse77,83,85. The gene discussed is CACNA1C; the disease is autism.