However, IL‐17A deficiency has been shown to prevent post‐myocarditis remodeling and progression to dilated cardiomyopathy by inhibiting the production of profibrotic molecules (e.g., IL‐1β, IL‐6, TNFα, and TGFβ1) and recruitment of myeloid populations.[203] These studies highlight the pivotal role of T cells in autoimmune fibrosis and suggest that targeting cytokines including IL‐17A, IL‐13, and IFN‐γ may represent a promising strategy for therapeutic intervention. This evidence concerns the gene IFNG and myocarditis.