And it was proved, for the first time, that some of BDNF functional deficits in Mecp2−/y mice can be overcome by selective A2AR activation, leading us to hypothesize that boosting BDNF signaling by increasing the availability of endogenous adenosine and/or the activity of A2AR could be a useful therapeutic strategy for RTT patients [15]. This evidence concerns the gene BDNF and Rett syndrome.