In combination with the increase in aldosterone levels found in Hyp mice (Figure 1E), we hypothesized that hypertension in aged Hyp mice may be due to crosstalk between FGF23 and RAAS signaling in the kidney and blood vessels, leading to a combination of volume overload through increased aldosterone and FGF23 secretion and increased peripheral vascular resistance by elevated angiotensin II levels. This evidence concerns the gene FGF23 and hypertensive disorder.