Hypertensive heart disease [5, 22, 23] can induce endothelial cell apoptosis [20] and activate NF-κB through myeloid differentiation gene response 88-dependent and -independent pathways by upregulating the expression of Toll-like receptor 4 (TLR4) on the surface of dendritic cells, initiating inflammatory cytokine transcription, mediating inflammatory mediator secretion, and producing oxygen-free radicals production [24]. This evidence concerns the gene TLR4 and heart disorder.