Recent proteomic studies have demonstrated the differential expression of proteins related to endothelial dysfunction and cerebrovascular complications of FD that respond to maintaining endothelial integrity (CRACD, HRG65), heme-hemoglobin metabolism, oxidative stress (TTHY, QSOX1, HEMO, CATA), and complement regulation (IGHG3, CO3, FCN2, FHR1) [53,61]. The gene discussed is CRACD; the disease is Fabry disease.