These include activation of RAAS, sympathetic nervous system overactivity, increased transforming growth factor-beta (TGFß) signalling, insulin resistance, uraemic toxins (e.g., indoxyl sulfate, p-cresyl sulfate), increase in cardiotonic steroids, oxidative stress and factors associated with CKD-MBD namely hyperparathyroidism, vitamin D deficiency, increased circulating fibroblast growth factor-23 (FGF-23), decreased Klotho expression and hyperphosphataemia [41, 164–166]. This evidence concerns the gene FGF23 and chronic kidney disease.