As the main effector of the RAS, Ang II activates AKT1-mTOR, TGF-β1-Smad2/3, NF-κB, and NADPH oxidase through Ang II type 1 receptor (AT1R), which in turn promotes fibrosis, inflammation, production of reactive oxygen species, and an abnormal ion channel function in the atrium, thereby leading to the occurrence of AF (Gao and Dudley, 2009; Hu et al., 2015). The gene discussed is NFKB1; the disease is atrial fibrillation.