Research examining genetic determinants to HTN therapy response have identified β1-adrenergic receptor (ADRB1), β2-adrenergic receptor (ADRB2), cytochrome P450 2D6 (CYP2D6), lysine deficient protein kinase (WNK), sodium-chloride symporter (SLC12A3), alpha subunit of the epithelial sodium channel (SCNN1A), alpha-adducin (ADD1), renin, angiotensin, angiotensin-converting enzyme (ACE), and angiotensin receptor variants as playing key functional roles in response to HTN therapy [12,16,24,25,26]. Here, SLC12A3 is linked to hypertensive disorder.