Gamma subunits are co‐ordinately regulated in response to metabolic requirements (Pinter et al. 2013), and it is likely that in the embryonic chick heart, PRKAG3 is expressed to compensate for the low levels of PRKAG2. Further, PRKAG2 has been associated with heart disorders such as cardiac hypertrophy, left ventricular dilation, supraventricular tachyarrhythmias, ventricular pre‐excitation and glycogen storage cardiomyopathies (Porto et al. 2016). This evidence concerns the gene PRKAG3 and cardiac hypertrophy.