Inflammatory cytokines such as IL-6 and TNF-α were added to isolated adipocytes, resulting in increased lipolysis and FFAs levels in several in-vivo and in-vitro studies [21, 22], also, elevated circulating FFA levels led to endothelial dysfunction in-vivo via activation of PKC-mediated inflammatory pathways and excess generation of oxidants [23, 24], which would partially explain the clinically demonstrated proarrhythmogenic potential of FFAs. The gene discussed is TNF; the disease is endothelial dysfunction.