Excessive ROS production in DCM activates TLR-4/MyD-88 signaling, resulting in cardiomyocyte apoptosis (110).Pharmacological inhibition of NOX in monocytes significantly reduces TLR2 and TLR4 mRNA and protein expression, and lower nuclear translocation of NF-κB is caused by pretreatment of neutrophils with the antioxidant N-acetylcysteine (111, 112). This evidence concerns the gene MYD88 and familial dilated cardiomyopathy.