At the cellular level, mutations in OCRL, which cause Lowe syndrome and the less severe Dent-2 disease, disrupt actin organization and lead to the formation of SNX9-mediated comet tails propelling clathrin-coated vesicles through the cytosol in patient fibroblasts (Nández et al., 2014). This evidence concerns the gene SNX9 and oculocerebrorenal syndrome.