Moreover, in Niemann-Pick type C1 (NPC1) disease, a lysosomal storage disease, the lipid accumulation in late endosomes alters the interaction between Rab9 and vimentin leading to protein kinase C inhibition, hypophosphorylation of vimentin, aggregation and localization of Rab9 to vimentin filaments causing late endosomes dysfunction [99]. Here, RAB9A is linked to lysosomal storage disease.