Mitochondrial dysfunction is a key feature of neuronal damage in AD, with impaired mitochondria causing energy production deficits and releasing reactive oxygen species (ROS) that induce oxidative stress and activate RIPK1/RIPK3/MLKL signaling, triggering necroptosis and worsening neuronal injury (Fu et al., 2021). The gene discussed is MLKL; the disease is Alzheimer disease.