In addition to blood leakage due to disruption of the BBB, which significantly upregulates the activation of microglia/macrophages (Khatri et al., 2012; Ozkul-Wermester et al., 2014) and astrocytes (del Zoppo et al., 2012), the elevated expression of the proinflammatory cytokines IL-1β and IL-6, the activation of their transcription factor NF-κB, and the expression of the inflammatory enzymes Cox-2 and iNOS are considered the chief mechanisms underlying HT. Here, NFKB1 is linked to hematocrit.