This assumption is based on the following observations: (1) knockout of PDE1A changes cAMP signaling in renal development, thereby progressing cystogenesis [16]; (2) in the present study, patients with the rs182089527 mutation showed cystic changes in the kidney and liver, as well as hypertension, typical clinical characteristics of polycystic kidney disease. The gene discussed is PDE1A; the disease is hypertensive disorder.