When the embryonic migration of gonadotropin-releasing hormone (GnRH) neurons from the nasal placode to their final destination in the hypothalamus is disrupted, the resulting phenotype is Kallmann syndrome, which is clinically characterized by hypogonadotropic hypogonadism and anosmia, while the term normosmic IHH (nIHH) denotes those IHH cases which not associated with anosmia/hyposmia (1). This evidence concerns the gene GNRH1 and Kallmann syndrome.