Therefore, the improvement in cognitive function in AD mice by low-dose HSP990 seems to be irrelevant to the mechanism reported by Wang et al. Conversely, only a low-dose Hsp90 inhibitor can lead to significant upregulation of EAAT2 levels, whereas a high-dose Hsp90 inhibitor caused transcriptional inhibition of EAAT2 (Figure S2), which raises doubts about whether the protective effects of high-dose Hsp90 inhibitor in AD mice can be attributed to EAAT2. The gene discussed is SLC1A2; the disease is Alzheimer disease.