RIPK3 and its substrate, MLKL, are essential for TLR and TNF receptor-mediated necroptosis7, 8, 9, 10, 11, 12, 28, 31, 41, and RIPK3 has been implicated in the inflammatory response in different disease models, including viral infection, retinal degeneration, brain and renal injury, and atherosclerosis6. Here, MLKL is linked to viral infectious disease.