Specifically, for CM, when taking into account the low level of EPCR expression in brain microvasculature, it is logical to suggest that the inhibition of IE binding to ICAM-1, a receptor that is expressed in micro vessels of human brain endothelial cells and is significantly inducible during various brain inflammations (reviewed in Reference [47]), including CM by TNFα (reviewed in Reference [48]), would be sufficient to block sequestration of these IE in the brain and improve the outcome or positively affect the pathology of CM. Here, PROCR is linked to brain inflammatory disease.