IGF1R and non-small cell lung carcinoma: While these mechanisms may operate independently of RTK signaling, the key roles of the wildtype or mutant EGFR as well as IGF-1R and other RTKs in NSCLC pathogenesis and therapeutic resistance80 raise the possibility that EHD1 overexpression may activate these pathways by sustaining RTKs, as we show in the EWS models.