Inflammation can induce oxidative stress, fibrosis, and thrombosis, resulting in changes in cardiac electrical, structural, and autonomic neurons, thereby promoting the formation of AF.[7–11] In comparison to patients with normal sinus rhythm, patients with AF exhibit elevated levels of inflammatory markers in their blood, including CRP, HSP β1 (also known as HSP27), IL-6, IL-8, and TNF.[9,11–15]. The gene discussed is IL6; the disease is atrial fibrillation.