These findings are particularly striking and suggest that androgen treatment may represent a means of stimulating BDNF/TrkB signaling, given the prevalence and severity of hypogonadism after SCI [91,92,93] and that the stimulation of motoneuron BDNF/TrkB signaling enhanced functional recovery in rodent SCI models [163]. This evidence concerns the gene NTRK2 and hypogonadism.