Instead of wholesale loss of Nkx3-2 expression, which would have been lethal in mice (Akazawa et al., 2000) or likely cause major defects similar to SMMD patients (Hellemans et al., 2009), our in situ hybridization data did not reveal qualitative differences in Nkx3-2 expression domains between Ctrl or LS embryos (Figure 4—figure supplement 2B). The gene discussed is NKX3-2; the disease is spondylo-megaepiphyseal-metaphyseal dysplasia.