Several studies have shown that hyperactivation of the TLR4 signaling pathway, which links myeloid differentiation primary response protein 88 (MyD88) with the activation of MAPK and NF-κB, and results in the expression of many proinflammatory factors, is an important mediator in DCM (102, 103). The gene discussed is TLR4; the disease is familial dilated cardiomyopathy.