Because both inflammation and PTH are suggested to mediate FGF23 levels in CKD, we employed a diet‐induced CKD model and showed that the −16kb enhancer mediates induction of Fgf23 in thymus, kidney, and bone and that this led to a blunting of the increase in iFGF23 levels in circulation at early onset of this kidney disease model. This evidence concerns the gene PTH and chronic kidney disease.