Our previous research has shown that the CRTC1-MAML2 fusion, a potential major oncogenic driver in MEC, induced autocrine AREG-EGFR signaling that supports MEC cell growth and survival, thus revealing anti-EGFR therapies as a potential anti-MEC strategy.11 Due to the common resistance associated with anti-EGFR therapies, identifying and blocking other critical signaling for tumor growth will have the potential in enhancing tumor responses and reducing resistance. The gene discussed is EGFR; the disease is neoplasm.