An example of how c-ABL can be activated is via TGFβ signaling; in idiopathic pulmonary fibrosis, c-Abl is activated by TGFβ (35), and silencing of c-Abl inhibits the pro-survival effects of TGFβ on myofibroblast apoptosis (34). This evidence concerns the gene TGFB1 and pulmonary fibrosis.