One possible mechanism where myocarditis and other autoimmune diseases could be induced and/or exacerbated by mitochondrial EVs is by activation of Toll-like receptor (TLR)4, interleukin (IL)-1β and leucin-rich repeat (LRR)-containing protein (NLRP)3, which is a pathway that has been demonstrated to increase myocarditis and viral replication in CVB3 models of myocarditis (88, 89). This evidence concerns the gene TLR4 and myocarditis.