In CHF mice injected with oe‐KDM3A + sh‐NC, the CHF was improved as reflected by the mitigated oxidative stress, inflammatory factor levels, pathological change and cardiomyocyte apoptosis, while the induction of BNIP3 reversed the therapeutic effects of elevated KDM3A on CHF through the result of a series of experiments (Figure 7F–R). The gene discussed is BNIP3; the disease is congestive heart failure.