In fact, both A-type (ANP) and B-type (BNP) NPs counteract the typical features of the ACE/Ang II/AT1R axis hyper-activation (endothelial dysfunction and increased permeability, pro-inflammatory, pro-hypertrophic, and pro-fibrotic activity), while experimental studies found that ANP can prevent the reduction in ACE2 mediated by Ang II and, conversely, Ang (1-7) can increase ANP release [34,41]. The gene discussed is NPPA; the disease is endothelial dysfunction.