Inflammation also promotes microvascular endothelial dysfunction and HF development (particularly HF with preserved ejection fraction) in experimental models, and proinflammatory cytokines (such as tumour necrosis factor-alpha [TNFα], interleukin-1β and -6) may reduce contractility and promote adverse LV remodelling [3, 24, 25]. The gene discussed is TNF; the disease is hydrops fetalis.