Moreover, the lysosome inhibitor NH4Cl, but not the proteasome inhibitor MG132, could greatly diminish the discrepancy in EGFR protein half-life in BSA-and BSA-PA/OA-treated CRC cells (Fig. 5C, D), suggesting that PA/OA treatment might impede the degradation of EGFR in a lysosome-dependent manner. The gene discussed is EGFR; the disease is colorectal carcinoma.