There have been limited therapeutic options for people who suffer from achondroplasia (ACH), one of the most genetically inherited types of skeletal dysplasia, resulting from the heightened Fibroblast Growth Factor Receptor (FGFR) 3 activation. Increased FGFR3 activity disrupts key molecular pathways involved in chondrocyte proliferation and differentiation. Such dysregulation in FGFR3 signaling alters chondrocyte function, impairing endochondral ossification. Currently available therapeutic options to treat ACH are limited and often suffer from side effects. Recently approved drug to treat ACH, vosoritide, while it enhances longitudinal bone growth in patients with ACH, fails to correct cranial abnormalities. One of them is foramen magnum stenosis, a condition that can result in severe neurological impairment or sudden death. Using tyrosine kinase inhibitors (TKIs) is an emerging alternative therapeutic approach for ACH. While TKIs generally exhibit favorable pharmacological properties and show promising results to correct both limb and cranial abnormalities in ACH mouse models, their use in therapeutic intervention is problematic; most FGFR TKIs exhibit low specificity among the FGFR1-4 variants and also inhibit some other non-FGFR receptor tyrosine kinases. The low selectivity among FGFRs and off-target activity contribute to the side effects and toxicity of FGFR-TKI therapies, thus limiting their use. Identification of alternative therapeutic solutions to treat patients with ACH is of interest.