Mice with cardiac-specific overexpression of Cav-3 exhibited augmentation of natriuretic peptide expression and nuclear Akt phosphorylation, resulting in reduced cardiac hypertrophy following TAC, with improved cardiac function and increased survival suggesting a potential therapeutic role for Cav-3 in heart failure (Horikawa et al., 2011). The gene discussed is AKT1; the disease is cardiac hypertrophy.