In that context, in an attempt to dissect out the role of Aβ in NPC pathogenesis, we characterized the gross phenotypes of Npc1 knockout (Npc1−/−/App+/+) and Npc1/App double knockout mice (Npc1−/−/App−/−) [9]; we reasoned that removing APP from the NPC brain could improve the disease phenotype because of the lack of Aβ and that this could unveil additional APP-specific mechanisms of neurodegeneration in NPC. This evidence concerns the gene APP and nasopharyngeal carcinoma.