Multiple constitutively active mutations of FGFR3 can lead to achondroplasia (ACH), one of the most common dwarfisms in humans, but the molecular mechanism remains elusive.In this study, we found that FGFR3 inhibiting AKT1 signaling contributes to the progress of bone development related to ACH.FGFR3 directly binds unphosphorylated AKT1, but not the constitutive activated form, to facilitate its degradation through CHIP-mediated ubiquitination pathway.Using in vitro embryonic bone culture system, we showed that BpV, a specific inhibitor of PTEN, increased the growth of cultured bone rudiment.Furthermore, we demonstrated that PTEN ablation in chondrocytes rescued the bone phenotype observed in FGFR3 knock-in mice by increasing chondrocyte proliferation and differentiation.Our findings reveal that FGF/FGFR3 plays an important role in the regulation of chondrogenesis and development of achondroplasia by booting the degradation of unphosphorylated AKT1.