If abnormal regulation occurs, myocardial fibrosis and remodeling can be observed.[34] Li Y et al found that mice with complete knockout of the THY1 gene showed more severe cardiac dysfunction and fibrosis,[35] and CCN2/CTGF (connective tissue growth factor) was strongly induced in HF.[36] Dorn L E et al found that CCN2 secreted by myocardial cells is not profibrotic, while CCN2 derived from fibroblasts can regulate cardiac fibrosis.[37] The second category is those involved in inflammatory responses, such as IL2, IL7R, CCL5, and CXCR4. This evidence concerns the gene CCL5 and Myocardial fibrosis.