Our previous studies have confirmed that overexpression of β-arrestin1 in the RVLM reduces BP and sympathetic outflow in hypertension by downregulating the expression of angiotensin type I receptors (AT1R) and revealed that this effect is mediated through the enhancement of interaction β-arrestin1 and IκB-α (Sun et al., 2018). The gene discussed is NFKBIA; the disease is hypertensive disorder.