Epicardial adipose tissue (EAT) is an active form of visceral adipose tissue that can affect myocardial function due to shared circulation with the myocardium. Given its rapid metabolic activity, EAT is considered a potential therapeutic target for medications that modulate fat and is a potent marker of metabolic changes including those observed in diabetic cardiomyopathy. Recent investigations propose an association between EAT accumulation and chronic diseases such as type 2 diabetes mellitus (T2DM), atrial fibrillation, and heart failure with preserved ejection fraction. According to the method first described by Iacobellis et al , EAT thickness is identified as the echo-free space between the outer wall of the myocardium and the visceral layer of the pericardium, measured in the parasternal short- and long-axis views at end-systole using ultrasound. Ultrasound of EAT is a safe, cost-effective, and readily available tool for cardiometabolic risk assessment. This minireview investigates the current role of echocardiography in the assessment of EAT thickness in patients with T2DM, regardless of the presence of overt heart failure. We also discuss whether changes in EAT thickness may be used as a significant marker of disease progression and if delta EAT thickness could serve as a surrogate of effective therapy.