A previous study showed that Api (20 mg/kg/day) administration significantly attenuated early brain injury, which includes brain edema, blood–brain barrier disruption, neurological deficiency, and cell apoptosis, after subarachnoid hemorrhage in rats by suppressing the expression of toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB), and their downstream pro-inflammatory cytokines in the cortex and by upregulating the expression of tight junction proteins of the blood–brain barrier (Zhang et al., 2015). Here, NFKB1 is linked to subarachnoid hemorrhage.