There is not yet convincing evidence for this discordance, but it can be hypothesized that, in PWS, although the missing paternal 15q11-q13 region includes the genes for the GABA receptor subunit cluster (GABRB3, GABRA5, and GABRG3) receptor, the maternal UBE3A is active, which could explain the lower rate of epilepsy in PWS [12]. This evidence concerns the gene GABRG3 and Prader-Willi syndrome.