We hypothesized that, upon NPC1-dysfunction, cholesterol-mediated sequestration of BACE1 within the endolysosomal system (where BACE1 is most active) causes enhanced cleavage of BACE1-substrates, and that increased BACE1-mediated proteolysis may also contribute to the pathological features of NPC disease. This evidence concerns the gene BACE1 and nasopharyngeal carcinoma.