In mouse models, the Class II HDACs HDAC9 and HDAC5 suppressed cardiac hypertrophy [11], and knockout mice lacking HDAC5 and HDAC9 showed spontaneous cardiac hypertrophy with age and in response to constitutive calcineurin activation or pressure overload due to aortic constriction [12]. Here, HDAC5 is linked to cardiac hypertrophy.