In support of this idea, PTH-KL−/− mice had altered transcript levels of several transcriptional regulators including Cfd, Smad4, Fabp4 and Pin1. The increased level of Pin1 in PTH-KL−/− mice is intriguing given its role in destabilizing PTH mRNA [32] and may represent yet another protective intracellular mechanism against hyperparathyroidism when FGF23-Klotho signaling is chronically disrupted. The gene discussed is SMAD4; the disease is hyperparathyroidism.