CYP2J2 and atrial fibrillation: Also, oxidative stress is viewed as an important inducer to atrial fibrosis and AF, and the modulation of EET on oxidative stress may be involved in suppressing AF.10 Furthermore, because of the limitations of the experimental AF model, and AAV9‐mediated CYP2J2 overexpression is not restricted to the atria, the reduction in AF susceptibility is inseparable from the blockade of CYP2J2/EET on cardiac remodelling, cardiac dysfunction and pro‐inflammatory cytokine formation.