This could explain the upregulation of GlcCer in NPC, where it acts as the glucose donor; the disparity in the isoforms of GlcCer between GD and NPC could be indicative of the GlcCer origin being either lysosomal in GD or endo-lysosomal in NPC, where the common C16 isoform may be the primary donor/substrate for GBA2 cholesterol glucosylation. The gene discussed is GBA2; the disease is nasopharyngeal carcinoma.