More broadly, the results of the present work give a clear indication that adjusting altered myocd expression to the range of physiological variation could be essential in order to reduce and normalize the expression of SRF/MYOCD-dependent SM-marker genes, that are upregulated in advanced HF of diverse etiologies ([27], [28], [29]; this work), without compromising the physiological functions of MYOCD signaling [17] as a part of the adaptive response of the heart to stress. Here, SRF is linked to hydrops fetalis.