Combined deletion of p38α and p38β results in cardiac defects during embryonic development (del Barco Barrantes et al., 2011), whereas p38γ/δ deficient mice exhibit reduced cardiomyocyte hypertrophic growth and smaller hearts (González-Terán et al., 2016), and cardiovascular disease is a common characteristic in premature aging syndromes (Carrero et al., 2016). This evidence concerns the gene MAPK11 and cardiovascular disorder.