TLR4 which leads to IL-1β production is a critical pathway in the pathogenesis of myocarditis, CAD, and MI (59, 61–63), and it may be this interaction between TLR4/IL-1β signaling on CD11b + immune cells (i.e., mast cells, macrophages) that elevates sST2 levels in males, where the ST2 receptor is cleaved to form sST2 in an effort to counteract IL-33. This evidence concerns the gene IL33 and myocarditis.