It is relevant to note here also the recent observation that gene therapy with the N-terminal proteolytic fragment of HDAC4, HDAC4-NT, overcomes CaMKII-induced cytoplasmic accumulation of HDAC4 and subsequent MEF2 activation after TAC, inhibiting not just the adverse LV remodeling after TAC but also the LVH (Lehmann et al., 2018), which clearly indicates a pro-hypertrophic role of CaMKII activation via HDAC4, independent of calcineurin. This evidence concerns the gene CAMK2G and persistent truncus arteriosus.