Recent preclinical and clinical data suggest that SGLT2is exerts cardioprotective effects through multiple mechanisms, including the modulation of inflammasome activity, specifically by reducing NLRP3 (NOD-, LRR-, and Pyrin Domain-Containing Protein 3) inflammasome activation and MyD88-dependent (Myeloid Differentiation Primary Response 88) signaling, which are critical drivers of cardiac inflammation and fibrosis. The gene discussed is MYD88; the disease is inflammation.