We additionally determined the effect of TNFAIP3-KO on the bacterial-induced activation of NF-κB signaling, and the immunoblotting showed that knock-out of TNFAIP3 in hBMECs significantly augmented the p65 phosphorylation as compared to wild-type hBMECs (Figure 4C), suggesting an intensified inflammatory response in TNFAIP3-KO cells along with the infection. Here, TNFAIP3 is linked to infection.