Thus, PRV CNS infection induces cerebrovascular dysfunction through the activation of pattern recognition receptor signaling pathways (e.g., TLR7) and acute inflammatory response genes (e.g., Havcr2 and IL1r1), the upregulation of endothelial apoptosis‐related pathways (e.g., caspase activity regulation), and the suppression of vascular development genes (e.g., Kdr, Cxcl12, and Tek). This evidence concerns the gene CXCL12 and acquired polycythemia vera.