The pleiotropic nature of uPAR interactions and function, uPAR structural flexibility, species specificity of the uPA-uPAR interaction, limitations of tumour models, the characteristic that uPAR expression is increased on tumour cells and tumour-associated stromal cells, and the baseline expression of uPAR in the glomeruli of normal kidneys that may result in potential “on-target off-tumour” toxicity are all the main hurdles to the development of uPAR inhibitors [72, 101, 147–152]. The gene discussed is PLAUR; the disease is neoplasm.