However, we must note that in another in vivo study, a pharmacological inhibitor preventing TNF-α binding to its receptor (namely CAS1049741-03-8) reduced post-infarction inflammatory response but worsened cardiac function due to enhanced cardiomyocyte apoptosis [213] possibly suggesting that TNF-α effect on cardiac contractility might be mediated by alternative pathways that might not include the binding of the cytokine to its receptors. The gene discussed is TNF; the disease is infarction.