Several heterogeneous mechanisms, such as de novo mutation, amplification, and downstream pathway activation of EGFR or the activation of bypass pathways (e.g., pathways involving c-Met, Axl, insulin-like growth factor receptor, and other members of the EGFR family), explain the acquired EGFR-TKI resistance in NSCLC [22–25]. The gene discussed is AXL; the disease is non-small cell lung carcinoma.