Therefore, firstly, cardiac‐specific overexpression of CYP2J2 was shown to reduce the AF inducibility in pathologic cardiac hypertrophy, and the mechanism may be attributed to decreased atrial fibrosis.16 Thereafter, enhanced EET level with sEHI treatment was also showed to reduce atrial arrhythmia susceptibility in TAC mice, by antagonizing inflammatory response.17 Likewise, we observed the susceptibility of AF in AAC mice was significantly decreased with AAV9‐CYP2J2 gene delivery, confirming that CYP2J2/EET is sufficient to prevent AF. The gene discussed is CYP2J2; the disease is atrial fibrillation.