In tumor cells, there are high-affinity binding sites or low-affinity binding sites by hGnRH-I and hGnRH-II; the dichotomy of the GnRH agonist and antagonist is not clearly present and the mechanisms activated by this receptor are different from those of the signaling pathways present in the pituitary–gonadal axis (96, 97, 102, 114–118). Here, GNRH1 is linked to neoplasm.