Serum potassium remained unchanged in Kl−/−/VDRΔ/Δ and was actually lower in Fgf23−/−/VDRΔ/Δ compared with wild-type and VDRΔ/Δ mice (Supplementary Fig S1B), ruling out hyperkalemia as the driving force for increased aldosterone secretion in compound mutant mice. Here, FGF23 is linked to Hyperkalemia.