Besides, lipid-derived excessive oxidants generation and impaired antioxidant capacity (inactivated NRF2-cascade) lead to redox imbalance and trigger inflammatory response (Li et al., 2019), which are in line with progressively deterioration of myocardial structure and function (Goldberg et al., 2012), including LA enlargement, and myocardial hypertrophy, connexin-43 remodeling, interstitial fibrosis in the atria (Harada et al., 2017). The gene discussed is NFE2L2; the disease is cardiac hypertrophy.