In FXS patients, the full-length isoform of bone morphogenetic protein type II receptor (BMPR2) was abnormally high and heterozygosity for BMPR2 or pharmacological inhibition of LIMK1 reduced the density of immature spines and restored synaptic function in FMR1 KO mice [235,236]. This evidence concerns the gene FMR1 and fragile X syndrome.