The over-activation of SGK1 has been shown to contribute to a variety of adverse outcomes, including renal fibrosis, lipid accumulation, and vascular dysfunction, which, in turn, can exacerbate metabolic dysregulation of calcium (Ca2+), phosphorus (P4+), parathyroid hormone (PTH), vitamin D, and fibroblast growth factor 23 (FGF23) [138]. This evidence concerns the gene FGF23 and renal fibrosis.