Consistently, genetic knockdown or pharmacological inhibition of JAK1 improved DCM-related phenotypes, whereas enforced JAK1 expression or pharmacological activation blunted the protective effects of CVB-D, indicating that CVB-D-mediated cardioprotection requires suppression of JAK1-STAT1 signaling.<h4>Conclusion</h4>Our findings indicate that CVB-D enhances mitochondrial function by suppressing the JAK1-STAT1 signaling axis, thereby ameliorating heart failure associated with DCM. The gene discussed is JAK1; the disease is heart failure.