EC necroptosis is activated by diverse ARDS stimuli, including allogenic red blood cells (98), hemin (99), heat stress (100), and endotoxin (through TLR4) (101), eliciting EC barrier dysfunction, in part through VE-cadherin disassembly and actin cytoskeleton remodeling (101). The gene discussed is TLR4; the disease is acute respiratory distress syndrome.