In vivo studies suggest there may be redundancy between PKN1 and PKN2 in cardiomyocytes, and double knockout of both kinases simultaneously in cardiomyocytes inhibits cardiac hypertrophy in pressure-overload conditions induced by transverse aortic constriction (TAC) or angiotensin II (AngII) [25]. The gene discussed is AGT; the disease is cardiac hypertrophy.