In mice with cardiac remodeling induced by TAC, S100A4-KO mice showed reduced interstitial fibrosis, reduced myofibroblasts, and inhibition of left ventricular collagen and pro-fibrotic cytokine expression, suggesting that blocking S100A4 may have therapeutic potential for cardiac hypertrophy and HF by alleviating cardiac fibrosis (Tamaki et al., 2013). The gene discussed is S100A4; the disease is cardiac hypertrophy.