The pharmacologically increased T will probably inhibit the secretion of GnRH and gonadotropins, at least on a system in which the low T levels should (and could) activate the eventual higher production of GnRH—and then LH—to enhance the natural synthesis of T. A relatively short androgenic drug treatment may allow for the ulterior recovery of testicular function [389], but excessively long-term treatments may induce more severe and enduring damage to the HHG axis regulation, affecting fertility and even inducing sterility [390,391]. The gene discussed is GNRH1; the disease is infertility disorder.