Lastly, we explored downregulators of the MAPK and STAT signaling pathways, which are activated downstream of FGFR3 activation and are responsible for defective chondrocyte differentiation and proliferation in FGFR3-linked chondrodysplasias.1,54 We found significantly higher expression levels of Dusp3 (coding for a downregulator of MAPK pathways60,61) in Fgfr3N534K/+ mice compared to control littermates (P = 0.04) (Fig. 5c). The gene discussed is SOAT1; the disease is chondrodysplasia.