Finerenone has been shown to attenuate adverse atrial remodeling related to CKD or T2DM, by inhibiting aldosterone activity, such as the prevention of fibrotic remodeling of the atrial myocardium via interfering with the small GTPase Rac1, limiting aldosterone/mineralocorticoid receptor-induced expression of the key profibrotic mediator connective tissue growth factor, and the collagen crosslinking enzyme lysyl oxidase, as well as microRNA-21, which enhances myocardial remodeling and fibrosis [5, 6, 51–54]. The gene discussed is CCN2; the disease is chronic kidney disease.