Moreover, modulating RYK function that has been shown to regulate stemness phenotype could enhance the efficacy of FGFR3 inhibition.[38] Combination therapies that target multiple RTKs as well as ECM remodeling enzymes such as heparanase can increase the efficacy of targeted therapies.[46] Therefore, tumor‐mimetic models that allow investigation of complex RTK signaling can serve as a reliable preclinical platform for developing efficient treatment strategies. Here, FGFR3 is linked to neoplasm.