It is possible, therefore, that a combination of PKD-independent mechanisms, such as the phosphorylation of class II HDACs by CaMKII [37,38] or GRK5 (G-protein-coupled receptor kinase 5) [39], or their redox-mediated nuclear export [20,40], or indeed HDAC-independent mechanisms mediated by p38-MAPK (mitogen-activated protein kinase) [41], ERK5 [42,43] or the acetyltransferase p300 [44], may be sufficient to induce significant MEF2 activation and thereby MEF2-driven transcriptional reprogramming towards cardiac hypertrophy. This evidence concerns the gene HDAC9 and cardiac hypertrophy.