Besides its effect in determining infarct size, TNF-α also contributes to post-MI cardiac dysfunction, remodeling, and onset of heart failure through increased oxidative stress, delayed resolution of inflammation, cardiomyocyte apoptosis, extracellular matrix, and collagen degradation mediated by MMPs, but also adrenoreceptor uncoupling and alteration of mitochondrial function [94, 164]. The gene discussed is TNF; the disease is heart failure.