TGFB1 and Camurati-Engelmann disease: Wang et al. (2013) used an osterix-Cre (Osx-Cre) transgene to delete Tgfbr2 in mesenchymal progenitors. They showed that Osx-Cre, Tgfbr2fl/fl mice have impaired tooth development and reduced mineralization of the mandible due to reduced osteoblast differentiation. In humans, genetic alterations leading to enhanced TGF-β signaling are associated with bone dysplasia in Camurati-Engelmann disease (Wallace and Wilcox, 1993). Of note, TGF-β regulates HSC quiescence and hematopoietic recovery following myeloablation (Brenet et al., 2013, Yamazaki et al., 2011, Zhao et al., 2014).