As macrophages digest apoptotic cells, various inflammatory cytokines, such as Tumor necrosis factor-α(TNF-α), Interleukin(IL)-1 β, IL-6, and transforming growth factor-β (TGF-β), may accumulate (35–37), promoting fibroblast activation, extracellular matrix (ECM) degradation, and increased matrix metalloproteinase (MMP) activity (38–40), further inducing cardiomyocyte apoptosis, autophagic damage, and fibrosis, eventually leading to cardiac hypertrophy (41). This evidence concerns the gene TNF and cardiac hypertrophy.