Several lines of evidence support this mechanism: (1) depletion of Arl4A promotes EGFR transport to lysosomes; (2) Arl4A depletion facilitates EGF-induced EGFR and NSCLC-related EGFR mutant degradation; (3) expression of Arl4A sustains EGFR ubiquitination levels; (4) Arl4A directly interacts with VPS36 in vitro and in vivo; and (5) and disrupting their interaction accelerates EGFR degradation. The gene discussed is VPS36; the disease is non-small cell lung carcinoma.