The potential mechanism of AS-IV in the treatment of MI might involve the downregulation of CaSR expression, upregulation of ERK1/2 phosphorylation (25), inhibition of nuclear NF-κB p65 subunit translocation to the nucleus (26), downregulation of TLR4/NF-KB expression (27), upregulation of HIF-1A expression (28), changes in Ca2+-ATPase activity (29), improvement in myocardial energy metabolism (30), and regulation of the mitochondrial apoptosis signaling pathway (31). This evidence concerns the gene NFKB1 and myocardial infarction.