In the mouse neuroblastoma model, NCYM overexpression increased beta-catenin levels (Suenaga 2014), and in bladder cancer lines, NCYM knockdown decreased beta-catenin levels and increased E-vimentin levels; these changes are characteristic of the EMT, and are consistent with an underlying mechanism in which NCYM inhibits GSK3B (Suenaga 2014) to stabilize its substrates, which include beta-catenein and E-vimentin. Here, VIM is linked to urinary bladder carcinoma.