Necroptosis can be activated by a plethora of internal and external stimuli, including the TNF superfamily members (e.g., Fas ligand (FasL), TNF-α and TNF-related apoptosis-inducing ligand (TRAIL)), interferon-γ (IFN-γ), bacteria, DAMPs, endoplasmic reticulum (ER) stress, hypoxia, LPS, metabolic and genotoxic stresses, ROS, viral infection and chemotherapeutic agents (91, 92). Here, FASLG is linked to viral infectious disease.