But surprising generalities are present as well: excluding Fragile X, all of cases so far studied involve the RhoA pathway, and in two instances (inflammation, Huntington Disease) this reflects a problem with BDNF “transmission.” In line with our expectation that this will hold for other models in which TBS-induced actin polymerization is impaired, it was recently reported that synaptic BDNF signaling through TrkB is markedly attenuated in Ube3a KO (Angelman syndrome) mice (Cao et al., 2013). This evidence concerns the gene BDNF and Angelman syndrome.