However, in vivo studies inhibiting or knocking out these subtypes selectively in cardiomyocytes fail to improve cardiac function in hypertrophy models, and in some cases exacerbate the problem [50,51,52,53]; in stark contrast to pre-clinical studies, where pharmacological p38 inhibitors are effective [7,8,42,43]. This evidence concerns the gene MAPK14 and cardiac hypertrophy.