Studies on mice have uncovered that genetic deletion of Nppa or its target receptor natriuretic peptide receptor A enhances cardiac hypertrophy and LV dilatation and deteriorates LV systolic function after TAC‐induced pressure overload,37, 38 while deletion of Nppb does not affect susceptibility for pathological cardiac hypertrophy.39 The gene discussed is NPPA; the disease is cardiac hypertrophy.