Although phenotypic similarities between the pug mutant, i.e., Xylt1-deficient mice, and our Slc10a7−/− mouse model suggest that the underlying mechanisms leading to growth defects are similar, i.e., premature chondrocyte maturation and early ossification32, further analyses of growth factor signalling pathways are necessary to fully understand the pathogenesis of the skeletal dysplasia induced by SLC10A7 deficiency. The gene discussed is XYLT1; the disease is skeletal dysplasia.