We have uncovered dissociation between JAK-STAT pathway activation, specifically STAT1, STAT3 and STAT5, and the anti-arrhythmic effects of empagliflozin in the in vivo rat heart, indicating that there may be an alternative prosurvival signal transduction pathway responsible for the protection of the myocardium against lethal reperfusion-induced arrhythmia. The gene discussed is SOAT1; the disease is Arrhythmia.