2011). Overexpression of the upstream p38 MAPK kinase (MKK) activators produces cardiomyopathy. Similarly, unrestrained activation of p38 leads to cardiac dysfunction (Wilkins et al. 2004; Auger-Messier et al. 2013). In addition, the ERK1/2 pathway promotes pathologic hypertrophy – constitutively active ERK1/2 leads to hypertrophy and cardiomyopathy, while ERK1/2 downregulation mitigates hypertrophic remodeling (Rose et al. 2010). Here, MAPK3 is linked to cardiomyopathy.