We reasoned that cholesterol-lowering strategies that rescue a prime pathological hallmark of NPC disease—accumulation of free cholesterol due to NPC1/2 dysfunction—may revert the retromer trafficking defect in NPC models and that cholesterol-loading in wt cells may, in contrast, cause retromer mistrafficking similar to that in NPC models. Here, NPC1 is linked to nasopharyngeal carcinoma.