In our model of mechanical unloading, we observed robust increases in Bnip3 (Figure 1K), a proapoptotic BH3‐only protein capable of inducing autophagy, mitochondrial dysfunction, and turnover in the context of several diseases, including cancer and cardiovascular disease.24–25 Similarly, Bnip3 was dramatically upregulated in FoxO3‐expressing hearts (Figure S1B), so we set out to evaluate its possible role as a required, downstream effector of FoxO3‐dependent cardiomyocyte autophagy. The gene discussed is FOXO3; the disease is cardiovascular disorder.