Under hypoxic conditions, uPAR contributes to theinitiation of EMT in a culture of human breast cancer MDA-MB-468 cells with anepithelial phenotype due to activation of different signaling mechanisms,including ERK1/2, PI3K/Akt, Src, and Rac1 [132, 133] .Preservation of the acquired mesenchymal phenotype of TSCs requires a highlevel of uPAR expression and is completely reversible upon suppression of uPARexpression, inhibition of the uPA–uPAR interaction, and blockade of PI3K,Src, and ERK1/2 signaling [132, 133]. The gene discussed is MAPK3; the disease is breast carcinoma.