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. Here, EGFR is linked to non-small cell lung carcinoma.