Thus, the recent results in Arf6 KO MEFs and in NPC1-null/mutant cells demonstrate that the altered distribution of PI4-kinases (PI4KIIα and PI4KIIIβ) and/or accumulation of PI4P could be central to altered intracellular cholesterol trafficking and retromer dysfunction in NPC disease. This evidence concerns the gene ARF6 and nasopharyngeal carcinoma.