The testis is descended through the processus vaginalis via propulsive force generated by the muscles derived from the gubernaculum. After propelling the testis, the smooth muscle should undergo programmed cell death for obliteration of the processus vaginalis. Achievement of programmed cell death mandates a transient decrease in sympathetic, but an increase in parasympathetic, tonuses. Since the sympathetic tonus is androgen-dependent, the decrease in androgen levels during the third trimester appears to be responsible for the process. Alterations in timing, intensity or duration of the decrease in sympathetic tonus under the control of the central nervous system give rise to hernia, hydrocele or abnormal testis localizations. The persistence of decrease causes undescended, retracted, or ascended testis. Absence or inadequacy of the decrease in sympathetic tonus results in rescue of more smooth muscle, thus inhibiting the obliteration. Inadequacy in the intensity or duration rescues less smooth muscle and gives rise to a hydrocele. Persistence of signals towards inducing programmed cell death contributes to decrease in fertility, and provides a basis for epididymo-vasal anomalies. The reduction in the central regulatory mechanism that involves catecholaminergic activity explains the blunting of luteinizing hormone (LH) response to gonadotropin-releasing hormone (GnRH).