The αMHC-promoter-driven overexpression of Mettl3 in cardiomyocytes was sufficient to induce physiological cardiac hypertrophy, while cardiac-specific deletion of Mettl3 exacerbated aging-related and pressure overload-induced cardiac remodeling in mice, concomitant with reduced cardiomyocyte hypertrophy [149]. The gene discussed is METTL3; the disease is cardiac hypertrophy.