Subsequently, detailed studies of Spry1−/− mice have revealed additional defects in multiple organs and cell types, including rostral cortex,6 mammary gland,7 mesenchymal stem cells8 and muscle satellite cells.9 These phenotypes are exacerbated by adding loss-of-function (LoF) alleles of other Spry genes (notably Spry2), indicating partial functional redundancy between Spry proteins.10 Depending on strain background, both increased and decreased skull size were documented in Spry1−/− mice, but craniosynostosis was not reported.11 The gene discussed is SPRY1; the disease is craniosynostosis.