Another study demonstrated that intravenous administration of serum from HF patients into wild-type mice induced left ventricular (LV) systolic dysfunction but concomitant addition of an inhibitor of IL-18, IL-18-binding protein (IL-18BP), was sufficient to prevent the development of cardiac dysfunction, thereby demonstrating that circulating cytokines derived from immune cells in the HF-damaged heart, can act as a carrier of inflammation between tissues [113]. The gene discussed is IL18; the disease is hydrops fetalis.