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. The gene discussed is ICAM1; the disease is brain inflammatory disease.