Studies in AF cohorts indicate that TLR signaling is upregulated, resulting in the production of pro-inflammatory and pro-fibrotic cytokines—including IL-6, IL-18, and IL-17A—which contribute to inflammation and subsequent structural and contractile remodeling processes in different stages of AF, such as ParAF and PerAF [145,146,147,148]. The gene discussed is IL17A; the disease is atrial fibrillation.