In addition, HED inhibited the nuclear translocation of NF-κB and Smads, and down-regulated the expression levels of transforming growth factor (TGF)-β1 and collagen I. These results suggest that HED could improve DCM by inhibiting the activation of NF-κB and Smads signaling to reduce myocardial inflammatory response. The gene discussed is NFKB1; the disease is familial dilated cardiomyopathy.