Hence, during the pathogenic process of DCM, the damaged cardiomyocytes induce inflammation, which recruits pro-inflammatory Th1, Th17, and other cell infiltrates that secrete pro-inflammatory IFN-γ and TNF-α as well as others to upregulate IDO expression in the lesion, including infiltrates and treated hUCMSCs. This evidence concerns the gene TNF and familial dilated cardiomyopathy.