The exacerbated LV dilation and dysfunction in these mice was found to be due to the combined contribution of augmented MMP-mediated proteolytic activities and heightened the TNFα-converting enzyme–TNFα pathway [147], while myocardial fibrosis was found to be mediated through an interaction between the TNFα and TGFβ pathways that led to increased expression of fibrillar collagens [148]. The gene discussed is TGFB1; the disease is Myocardial fibrosis.