In mice heterozygous for Crebbp, the gene mutated in Rubinstein-Taybi syndrome (57), HDAC inhibition with trichostatin A (TSA) rescued defective neurogenesis in cortical precursors (58), and vorinostat treatment improved long-term potentiation and fear-conditioning memory defects (59). The gene discussed is HDAC9; the disease is Rubinstein-Taybi syndrome.