Activated p38 phosphorylates several hypertrophic transcription factors, such as MEF2.56 TAK1 and p38 activation can be observed in cardiac hypertrophy models induced by pressure overload, ET-1 or PE.57–60 Overexpression of an activated TAK1 mutant in cardiomyocytes led to p38 phosphorylation in vivo, cardiac hypertrophy, fibrosis, and eventually heart failure.60 Dual-specificity protein phosphatases (DUSPs) are a family of specialized phosphatases that can dephosphorylate MAPKs and inactivate them.61 Among them, DUSP1 and DUSP4 mainly act on p38. This evidence concerns the gene MAPK1 and heart failure.