Finally, a recent proteomic analysis of urinary and tissue-exudative extracellular vesicles has demonstrated that MARCKS and MARCKSL1 are significantly upregulated in bladder cancer patients [61], and phorbol 12-myristate 13-acetate (PMA)-induced hyperphosphorylation of MARCKS inhibits invasiveness in bladder cancer cells by modulating the cytoskeletal structure [62]. The gene discussed is MARCKSL1; the disease is urinary bladder cancer.