Therefore, we again generated anti‐human HMGB1 human monoclonal antibody, which has a high affinity to human HMGB1, cross‐reacts with mouse HMGB1, suppresses the interaction between mouse/human HMGB1 and TLR4, and revealed that, even after the onset, administration of the anti‐human HMGB1 human monoclonal antibody rescued the cognitive impairment of the AD model mice (Okazawa, Patent Application: 20190211092 16/324192). The gene discussed is HMGB1; the disease is Cognitive impairment.