Moreover, CCR9 gene knockout reserves the conduction function and the expression of Cx43 in myocardial tissue after MI, suggesting that CCR9 knockout diminishes the inflammatory response and fibrosis, which can consequently save some Cx43 expression from MI induced degradation, and thus alleviated the electrical uncoupling and conduction abnormalities among myocardial cells. The gene discussed is CCR9; the disease is myocardial infarction.