With regard to the mechanism how ANP suppressed ISO-induced mitochondrial ROS generation, for which we have no evidence in the present study, the beneficial effects of ANP might be due to preserved mitochondrial biogenesis which is significantly affected in pathophysiological conditions such as HF and hypertrophy [33] and/or reduced mitochondrial ROS-induced mitogen-activated protein kinase (MAPK) signaling as shown in phenylephrine-treated cardiomyocytes [34]. The gene discussed is WNK2; the disease is hydrops fetalis.