Among the mechanisms by which cancer cells become resistant to reversible EGFR-TKIs are 1) gatekeeper mutations in EGFR, such as the T790M second mutation [7,8]; 2) activation of bypass signaling caused by Met amplification [9], hepatocyte growth factor (HGF) overexpression [10], or Gas6-Axl activation [11]; 3) activation of downstream molecules (PTEN loss or PIK3CA mutation) [12,13]; 4) small-cell lung cancer transformation [14]; and 5) epithelial-to-mesenchymal transition [15]. The gene discussed is EGFR; the disease is cancer.