Our recent study reported that the conduction tissue-specific loss of Ndufs4 (driven by HCN4-Cre) in mice is sufficient to cause similar arrhythmia in a cell-autonomous manner, although the metabolic defect of Ndufs4−/− in neurons, cardiomyocytes, and the other cell types in the hearts (e.g., inflammatory cells [22,23]) could also contribute to arrhythmia by impacting the neurohormonal or paracrine regulation of cardiac rhythm [24]. The gene discussed is NDUFS4; the disease is cardiac arrhythmia.