Out of the modeled patients, we selected the CREBBP-mutated patient 149 (aka P149), who harbors exon 18 c.3474 G>A, p.(Trp1158ter) truncating mutation and manifests the most severe ID [7] to assess whether short- and long-term exposure of his iPSC-derived neural progenitors to TSA might ameliorate the morphological and electrophysiological alterations exhibited by young and mature neurons from characterized RSTS patients [18]. The gene discussed is CREBBP; the disease is Rubinstein-Taybi syndrome.