Smoc1 has been previously identified as a causative gene for human anophthalmia and microphthalmia,18–20 and zebrafish MO knockdown experiments generated a small eye phenotype but lacked a coloboma.19 Knockdown of zbtb4 in zebrafish embryos showed high embryonic mortality (90%) with surviving morphants exhibiting early developmental defects, including microcephaly, which would prevent potential identification of eye defects.21 Therefore, both genes were excluded from further analysis. Here, ZBTB4 is linked to Anophthalmia.