Previous studies have shown that activation of the TGF-β/Smad pathway by inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, can enhance the expression of the myocardial fibrosis biomarker, α-SMA, and myocardial hypertrophy biomarker, β-MHC, induce the production of collagen and extracellular matrix, and subsequently lead to conditions, such as myocardial hypertrophy, myocardial interstitial fibrosis, and ventricular remodeling (11, 27, 28). This evidence concerns the gene ACTA1 and cardiac hypertrophy.