The increased cardiovascular risk after influenza infection can be explained by several mechanisms, including the destabilization of atherosclerotic plaque, increased macrophages in the circulation, proinflammatory molecules, such as tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), and sympathetic activation [3,36,37,38,39,40,41,42,43]. The gene discussed is TNFSF12; the disease is influenza.