Mechanistic explanation for pioglitazone-induced protection against AF comes from an in vivo study, which demonstrated that this drug significantly reversed β1-Aab-induced AF susceptibility, improved atrial structural remodeling, reduced systemic IR, and enhanced the expression of key glycolipid transport proteins: glucose transporter 1 (GLUT1), CD36, and carnitine palmitoyltransferase Ia (CPT1a). Here, CD36 is linked to atrial fibrillation.