To evaluate which pathway of degradation is activated by erlotinib in TKI sensitive lung cancer cells, HCC827 cells were treated with erlotinib (3 μM) for 12 h and then exposed to MG132, to inhibit proteasomal activity, or to 3-methyladenine (3-MA to block lysosomal function, followed by immunoblotting to assess rescue of EGFR protein levels. The gene discussed is EGFR; the disease is lung carcinoma.