Growth impairment in CKD children has been explained mainly by a reduced IGF-I bioavailability, in part owing to a GH-resistance state caused by a postreceptorial defect in the JAK2-STAT5b signaling pathway downstream of the GH, as shown in the liver, skeletal muscle, and GP [3,17,18,19,20]. This evidence concerns the gene JAK2 and chronic kidney disease.