p38 is activated in the vessel wall in response to pressure overload, hypoxia and heart failure (Kyriakis and Avruch, 2001; Hoefer et al., 2010) and also by neurohormonal stimuli such as angiotensin II or endothelin-1; both associated with vasoconstriction and ventricular remodeling (Vijayan et al., 2004; Kumar et al., 2008). Here, MAPK1 is linked to heart failure.