It is also noteworthy that the TMS alterations common to FXS and GABRG2(R43Q) patients differ markedly from those seen in disorders involving other aspects of the GABAergic system, including patients with succinic semialdehyde dehydrogenase (SSADH) deficiency25, who lack an enzyme involved in GABA metabolism, and Prader-Willi syndrome, caused by deletion or imprinting defect of genes encoding α5, β3, and γ3 subunits of GABAA receptors64. This evidence concerns the gene GABRG2 and Prader-Willi syndrome.