Altogether, most reports show an active role for uPAR in EMT, even though a recent report shows that, instead, uPAR expression is essential for maintaining the epithelial phenotype in neuroblastoma Neuro2a cells, since uPAR silencing induces the down-regulation of epithelial markers (E-cadherin, occludin, and claudin-5) and the increase of mesenchymal markers (N-cadherin, α-smooth muscle actin, and interleukin-6) [70]. Here, PLAUR is linked to neuroblastoma.