Necroptosis (programmed necrosis) occurs in response to TNF, Fas, or TRAIL, as well as certain TLR ligands, when caspase activity required for apoptosis is blocked. Necroptosis is typically considered a highly pro-inflammatory mode of cell death, due to release of intracellular "danger signals" that promote inflammation. However, because most pro-necroptotic stimuli are intrinsically highly pro-inflammatory—due to their ability to initiate the synthesis of numerous cytokines and chemokines—the inflammatory consequences of necroptosis are complex. Here, we suggest that necroptosis might have anti-inflammatory effects in certain settings, through curbing excessive TNF- or TLR-induced inflammatory cytokine production.