The primary functional source of CGRP was reported to be independent of the kidney, because chemical denervation of renal sensory afferents removed tissue CGRP but without any beneficial effect in hypertensive mice.46 However, our study highlights that mimicking sensory nerve efferent function by using an αCGRP analogue protects against end-organ damage in hypertension, especially renal fibrosis, a strong predictor of clinical progression of kidney disease. This evidence concerns the gene CALCA and renal fibrosis.