As we have recently discovered that Yes-associated protein (YAP)-dependent primary necrosis of cortical neurons at the ultra-early stage of AD37 is identical to transcriptional repression-induced atypical cell death (TRIAD)61, and that it is followed by secondary necrosis of neighboring neurons with unknown characteristics and extracellular Aβ aggregates as ghost of cell death37, we examined how PKC inhibitor and human monoclonal anti-HMGB1-Ab #129 affect the two types of necrosis and extracellular Aβ aggregates in AD model mice (Fig. 6f). This evidence concerns the gene HMGB1 and Alzheimer disease.