The activation of myeloid differentiation factor 88 (MyD88)-dependent toll-like receptor 4 (TLR4) signaling pathway can promote the expression of interleukin-1 receptor-associated kinase, nuclear factor-κB (NF-κB), and AP-1, and thus lead to the production of a large number of inflammatory factors, such as cyclooxygenase-2 (COX-2), IL-1 and IL-6, which are associated with hypertension-induced endothelial damage. Here, NFKB1 is linked to hypertensive disorder.