The observation that overexpression of RAB-5 could promote the lysosomal degradation of accumulated polycystin-2 in BBSome-deficient cilia suggest that positive modulation of the downstream lysosomal system could be a novel therapeutic avenue for BBS disorders, and potentially other ciliopathies that share similar pathogenesis mechanism with BBS. This evidence concerns the gene PKD2 and Bardet-Biedl syndrome.