Phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and ERK1/2, the downstream of FAK, are the two classical signaling factors that directly cause myocardial fibrosis [51,52], and can result in the α-SMA-positive myofibroblast diversity and the formation of various types of collagens. This evidence concerns the gene PTK2 and Myocardial fibrosis.