Moreover, it should be the subject of future studies to assess whether patients with LOY will particularly benefit from therapies modulating profibrotic mechanisms such as sodium-glucose co-transporter 2 inhibitors,46 selective non-steroidal mineralocorticoid receptor antagonists,47 or novel anti-fibrotic therapeutic approaches including specific inhibitors of TGF-ß.48 Furthermore, the findings on the interaction between LOY and the wGRS for myocardial fibrosis should be independently replicated. The gene discussed is NR3C2; the disease is Myocardial fibrosis.