Physiological cardiac growth is a feature of normal postnatal development in which an increase in cardiac muscle cell diameter is observed as infants mature to adults. 1 This nonpathological heart growth, sometimes referred to as physiological hypertrophy, 2 is similar to the growth observed in the hearts of trained athletes in whom the adaptation to increased workload leads to increased vascularization of the myocardium and more forceful ejection. 1, 3 In contrast, pathological hypertrophy occurs in patients with hypertension or valvular heart disease. A number of molecular distinctions can be made between physiological and pathological cardiac hypertrophy. For example, pathological cardiac hypertrophy is associated with interstitial fibrosis, activation of a fetal gene program, and myocyte apoptosis, whereas physiological cardiac growth does not display these features. Most studies have focused on elucidating mechanisms of pathological heart growth, whereas the molecular regulation of physiological cardiac growth is less understood. In this issue of Circulation, an article by DeBosch et al4 sheds light on the role of Akt1 signaling in the promotion of physiological growth and inhibition of pathological hypertrophy.