The results indeed depicted inhibition of FGFR3 signalling, and RBM-007 also repaired defective chondrocyte differentiation in tibial organ culture, in vitro and in vivo ACH chondrocyte differentiation, as well as skeletal defects in the ACH mice model, suggesting that RBM-007 is potentially useful in ACH and other FGFR3-related skeletal dysplasia therapy (Kimura et al., 2021). The gene discussed is FGFR3; the disease is skeletal dysplasia.