These negative results may be explained by the specific characteristics of the inflammatory cascade that contributes to HF pathophysiology, such as [30,31]: (1) a chronic, low grade systemic inflammation, that is induced by multiple mediators besides TNF-α and IL-1β, such as damage-associated molecular patterns (DAMP) and mitochondria injury, which arise in the setting of myocardial dysfunction; (2) promotion of cell survival and beneficial tissue remodeling by low levels of TNF-α; (3) a by-stander, as opposed to a pathogenic role, of increased cytokine levels seen in HF. This evidence concerns the gene IL1B and hydrops fetalis.