Inhibition of pro-inflammatory cytokines, like IL 17A, decreases the atrial expression of IL-6, IL-1β and TGFβ, along with the levels of type I collagen, type III collagen, and α-smooth-muscle actin (αSMA), and increases the amount of MMP2 and MMP9, thereby reducing fibrosis and the duration of inducible AF episodes [56,57]. The gene discussed is IL1B; the disease is atrial fibrillation.