TLR signaling pathways occupy a key role in this mechanistic crosstalk, taking into account that enhanced sympathoexitation and BP elevation have been shown as a result of TLR activation, mainly TLR4 [40] In fact, among all TLRs, TLR4 is constitutively and abundantly expressed in the CNS, and its role in promoting inflammation and vascular dysfunction has been well-demonstrated in several experimental models from normotension to hypertension [41,42]. The gene discussed is TLR4; the disease is Hypertension.