Although it is well established that FGFR3-activating mutations in chondrodysplasia primarily affect CCs and that changes in the proliferation and differentiation of these cells are responsible for the defective elongation of long bones (Ornitz and Legeai-Mallet, 2016), several observations in humans and in animal models suggest that OBs are also affected by elevated FGFR3 signaling. The gene discussed is FGFR3; the disease is chondrodysplasia.