Generation and in-depth characterization of multiple CBP-deficient strains, including Cbp+/−, conditional knock-out (cKO) mice, and transgenic mice expressing a dominant negative allele, provided important clues to unravel the etiology of RSTS and to demonstrate the contribution of CBP/p300 to cognitive functions both during development and adult life [11–13]. The gene discussed is CREBBP; the disease is Rubinstein-Taybi syndrome.