In the acute phase after myocardial infarction (MI), CFs respond to proinflammatory stimuli (e.g., reactive oxygen species (ROS), interleukin (IL)-1, and tumour necrosis factor alpha (TNF-α)) in the ischemic microenvironment by altering their gene expression profile and acting as inflammatory supporter cells [6]. The gene discussed is TNF; the disease is myocardial infarction.