An early study demonstrated that angiotensinogen (AGT), the primary substrate of the renin–angiotensin–aldosterone system (RAAS), was able to affect miR-21 expression, and its overexpression resulted in a rise in aldosterone secretion and cell proliferation, implicating the changes in miR-21 expression levels causing primary aldosteronism and hypertension [120]. The gene discussed is AGT; the disease is primary aldosteronism.