Genetically inducing renal-specific lymphangiogenesis in mice prevented the development of salt-sensitive hypertension, nitric oxide inhibition (L-NAME)-induced hypertension (LHTN), and angiotensin II-induced hypertension (A2HTN), and this was associated with a reduction in renal immune cell accumulation and increased sodium excretion [9,11,12]. The gene discussed is AGT; the disease is Hypertension.