In xenograft tumor models that harbor FGFR aberrations including FGFR3-driven UMUC14 model, intratumoral MYC protein level was profoundly decreased along with the strikingly inhibited tumor growth due to FGFR blockade in responders while in an FGFR-nonresponsive model, the intratumoral level of MYC following FGFR inhibitor treatment remained constant, regardless of the abolishment of FGFR signaling [136]. Here, MYC is linked to neoplasm.