The only evidence to date that implicates the uPA/uPAR pathway to human malaria pathogenesis comes from a post-mortem study of patients with CM that reported increased expression of uPAR on macrophages, microglial cells, astrocytes, and endothelial cells in CM-associated lesions, suggesting that uPAR may contribute to blood–brain barrier disruptions and immunopathology in CM (38). This evidence concerns the gene PLAU and cutaneous mastocytosis.