Due to the mutations' positions in the FoxH1 polypeptide and the failure of both mutant proteins to activate a luciferase reporter linked to FoxH1 binding sites [17], the sur alleles have been assumed to represent null mutations of FoxH1. However, embryos possessing both maternal and zygotic sur alleles display only mild versions of FoxH1 loss-of-function phenotypes observed in other organisms, including variable deficiencies in axial mesoderm and floor plate, as well as variable degrees of synopthalmia/cyclopia [15], [16]. The gene discussed is FOXH1; the disease is holoprosencephaly.