This finding suggests that desmin might be cleaved by overexpression of TNF-α, which leads to development of a dilated cardiomyopathy that recapitulates the classical transition to failure with progressive LV dysfunction and remodeling, cardiac myocyte hypertrophy, interstitial fibrosis, and progressive myocyte loss during the HF process [29]. The gene discussed is TNF; the disease is dilated cardiomyopathy.