The exact mechanism of TDS is unknown, but suppression of testosterone production, androgen receptor expression, or Leydig cell function in the foetal testis has been associated with subsequent reproductive impacts in adulthood, including cryptorchidism, hypospadias, dysfunctional testis, as well as testicular cancer and impacts on fertility (Skakkebaek et al., 2001; Sharpe, 2003). Here, AR is linked to cryptorchidism.