Comparable with a study reporting that blockade of MEF2 acetylation can permit recovery from pathological cardiac hypertrophy without impairing physiologic adaptation (Wei et al., 2017), the lower concentration and reduced activity of MEF2A that we found in Trpm4 cKO TAC hearts suggest that inhibition of TRPM4 channels is potentially a viable therapeutic option for reducing pathological hypertrophy in response to pressure overload. Here, MEF2A is linked to cardiac hypertrophy.