Other studies using mice with a specific deletion of FGFR1 in distal tubule segments have suggested that FGF23 activates FGFR1/alpha-Klotho complexes in the distal tubule leading to an increase of sodium-chloride symporter (NCC)-dependent sodium (Na) reabsorption, a decrease of Ace2 and renal KIotho, leading to increased blood pressure and hypertension (119). Here, ACE2 is linked to hypertensive disorder.