Other studies confirmed that the defects observed in the myelination process in NPC are due to an inhibition of OLs maturation rather than to a reduction in their number [49,50], and this mechanism was observed in other models of NPC; in fact, the NPC1nmf164/nmf164 mouse strain (characterized by the substitution of aspartate to glycine in NPC1 protein) also shows a decrease in the expression of the myelin basic protein (MBP), a well-established marker of mature myelin, in the cerebellum (the most affected brain area in NPC) [51]. This evidence concerns the gene NPC1 and nasopharyngeal carcinoma.