Changes in functional demand can alter the morphology of the adult heart;for example, pressure overload can induce ventricular hypertrophy. Now, two groups of researchers provide evidence that blood flow also affects cardiac morphology during embryogenesis. Berdougo et al. have investigated the effect of a mutation in the gene atrial myosin heavy chain on heart development in zebrafish (see p. 6121). Although this gene is expressed only in the atrium, mutations in it result in not only atrial contractile defects but also ventricular morphological defects. Similarly, Huang et al. report that inactivation of the gene for atrial myosin light chain 2 in mice causes severely diminished atrial contraction and secondary abnormalities in cardiac morphogenesis (see p. 6111). Both research teams conclude that alterations in blood flow caused by the mis-functioning of one embryonic heart chamber epigenetically influence the morphogenesis of the other chamber, and they discuss how these findings may provide clues to the causes of human congenital heart defects.