BMPR1B and Anophthalmia: Whereas targeted deletion of Bmpr1b alone disrupts the ability of many ventrally located ganglion cells to enter the optic nerve head [88], conditional Bmpr1a-/fx/Bmpr1b-/-;cre double mutant embryos exhibit more profound structural abnormalities due to excess apoptosis and reduced proliferation at E11.5, and show anophthalmia at birth [61].