Indeed, NOX activity and p47phox membrane localization are increased in human cardiomyopathy [5] and NRCMs expressing dominant-negative Rac1T17N or with siRNA-mediated knockdown of Nox2 are protected from AngII-induced ROS generation and cardiomyocyte hypertrophy [69], suggesting Rac1/NOX2 signaling is critical for AngII-induced cardiac hypertrophy. The gene discussed is AGT; the disease is cardiac hypertrophy.