In contrast to the effects of such mutants on other cell lineages, they did not activate malignant transformation of cardiomyocytes, but instead induced cardiac hypertrophy the with expression of classical markers of pathological hypertrophy such as Atrial Natriuretic Factor (ANF), Skeletal Muscle α Actin (SkM-α Actin), β-Myosin Heavy Chain (β-MHC) and c-Fos in neonatal cardiomyocytes in vitro [5, 14, 15]. Here, NPPA is linked to cardiac hypertrophy.