Ligand binding to EGFR leads to endocytosis of EGFR, and the internalized EGFR is sorted for recycling back to the cell surface or targeted for lysosomal degradation to attenuate persistent EGFR signaling.6, 7 Internalization-defective EGFR mutants may escape the ligand-induced lysosomal degradation pathway, leading to prolonged cell signaling and tumor development.8 Therefore, activation of EGFR endocytosis and downregulation of EGFR are considered to be therapeutically relevant in cancers.7, 9. The gene discussed is EGFR; the disease is cancer.