HDAC4 and cardiac hypertrophy: In response to adverse stimulation, CaMKIIδB reduced HDAC4 phosphorylation and transport from the nucleus to the cytoplasm, thereby inducing increased levels of nuclear HDAC4, resulting in dissociation of the complex HDAC4/SUV39H1, demethylation of H3K9, transcriptional activation of Mef2, and ultimately cardiac hypertrophy (67).