Instead, we found that TSA slightly increased the level of monomeric ubiquitin in the hippocampus of WT mice, which shared a number of similarities with Tian et al.’s [37] findings that chronic TSA treatment increased monomeric ubiquitin level, including ubiquitin B and ubiquitin A. We also justified that APP/PS1 mice had a much higher level of ubiquitin monomer relative to WT mice, which was in line with previous results by Tseng and colleagues [38] in which proteasomal dysfunction resulted in the increases of Aβ accumulation and monomeric ubiquitin in AD mice brains. The gene discussed is APP; the disease is Alzheimer disease.