The ATG MO-mediated knockdown of endogenous zebrafish Cyp1b1 showed improvement of craniofacial defects, but did not statistically significantly decrease the percentage of embryos with colobomas and craniofacial defects (36.4 ± 17.0, P = 0.06) due to human CYP1B1 overexpression (Figs. 8C, 8C'). The gene discussed is CYP1B1; the disease is coloboma.