In addition to its proinflammatory function, excess TNF-α also triggers neuronal necroptosis, as another source of neuronal loss in AD brain, through activation of the receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1/3) and the mixed lineage kinase domain-like (MLKL), which can be inhibited by intracerebral injection of TNF-α neutralizing antibody or by downregulation of SQSTM1 (p62) [12, 13]. The gene discussed is RIPK1; the disease is Alzheimer disease.