DHCR7 and Smith-Lemli-Opitz syndrome: Dhcr7Δ3-5/T93M mutant mice, a hypomorphic mouse model of SLOS, are heterozygous for a targeting vector to disrupt Dhcr7 via a neomycin insertion, with deletion of coding exons III, IV and part of V, along with a dinucleotide mutation in codon 89 of Dhcr7, resulting in an ACA (Thr) to ATG (Met) change (Correa-Cerro et al., 2006; Wassif et al., 2001).