In NC or miR-125b inhibitor–treated primary neuron AD model (Figures 5A–F), as well as in NC or miR-125b inhibitor–treated PC-12 cellular AD model (Figures 5G–L), Si-FOXQ1 decreased FOXQ1 expression and neurite outgrowth and increased cell apoptosis, while Si-FOXQ1 did not affect miR-125b expression (Figures 5A–L, Supplementary Figure 3); meanwhile, Si-FOXQ1 also upregulated TNF-α, IL-1β, and IL-6 levels (Figures 6A–F). This evidence concerns the gene TNF and Alzheimer disease.