This phenomenon has been confirmed in multiple studies on patients with GH deficiency, Turner’s syndrome, neonates born small for their gestational age, and children with idiopathic short stature.5,8,22,23 These studies have demonstrated increased responsiveness to recombinant human GH therapy in homozygous d3d3 genotype carriers compared to that in fld3 or flfl genotype carriers, as indicated by accelerated longitudinal bone growth and increased final height. This evidence concerns the gene GH1 and Turner syndrome.