This is consistent with our earlier work showing an essential role for these p38 isoforms in mTOR-dependent physiological and pathological cardiac hypertrophy (González-Terán et al., 2016), as well as with previous reports indicating that p38α does not mediate hypertrophic responses in animal models of pressure-overload cardiac hypertrophy (Nishida et al., 2004). Here, MAPK14 is linked to cardiac hypertrophy.