Conversely, inhibition (KO) of CNP/GC-B/cGMP signaling in endothelial cells provoked endothelial dysfunction, with mild thickening and stiffening of the aortic wall, increased systolic BP, enhanced atherosclerosis in aortic roots, and impaired post-ischemic angiogenesis. The gene discussed is NPR2; the disease is endothelial dysfunction.