Notably, excess fibroblast growth factor-23 (FGF23) coupled with reduced Klotho, as well as skeletal resistance to PTH due to disrupted Wnt–β-catenin signaling (exacerbated by uremia-related intestinal dysbiosis), have all been implicated in maintaining hyperparathyroidism in CKD [2]. The gene discussed is FGF23; the disease is hyperparathyroidism.