Here, our results demonstrated that the treatment of mice with LDN significantly inhibited the Ang II-induced activation of AKT, ERK1/2, HIF-1α, TGF-β/Smad2/3, IL-1, IL-6, and NOX, thereby leading to the improvement of atrial remodeling and AF (Figs. 4–6). The gene discussed is HIF1A; the disease is atrial fibrillation.