NPR2 and achondroplasia: The significance of this aspect of FGF signaling for ACH was definitively established by the recent finding that, in a mouse model of ACH, bone growth is restored by replacing the NPR2 protein with a dephosphorylation resistant form of NPR2 (NPR27E/7E, also known as GC-B7E/7E) with a modified version of the protein that cannot be dephosphorylated (30).