The chronic inflammation in patients with heart failure, characterised by elevated levels of pro-inflammatory molecules such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and C-reactive protein (CRP), triggers atrial fibrosis, enlargement, and cell death, disrupting the normal organisation and function of atrial tissue and leading to the development and maintenance of AF. Here, IL6 is linked to atrial fibrillation.