The important role of NO in the regulation of (medullary) renal blood flow and (tubular) sodium excretion has been recognized for a long time and it has been postulated that inhibition or deficiency of NOS would result in sustained hypertension.30 Thus, while renal dysfyunction is not the initial cause of hypertension in patients on VEGF inhibitor therapy, inhibition of renal NO signaling is associated with a rightward shift of the renal pressure-natriuresis curve, impaired sodium excretion, and consequently fluid retention and salt-dependent hypertension.14 The gene discussed is NOS1; the disease is hypertensive disorder.