Alpk3+/– heterozygote mice had normal contractile function, fertility, and survival, but developed significant ventricular hypertrophy beyond 1 year of age, supporting the pathogenicity of Alpk3 heterozygote variants in adult human patients (Figure 3E, mean LV posterior wall thickness age 51 to 90 weeks: Alpk3+/– (n=20)=0.95 mm versus WT (n=16)=0.77 mm; P=7.0×10-10). The gene discussed is ALPK3; the disease is Ventricular hypertrophy.