Herein, several possible explanations were proposed: (i) FOXQ1 might transactivate gene expression of p21 (G1 cyclin kinase inhibitor), which arrested cells in G0/G1 phase, promoted neurite outgrowth, and repressed cell apoptosis in AD; thereby, FOXQ1 inhibition enhanced cell apoptosis and inflammation but repressed neurite outgrowth (Park et al., 2012). Here, FOXQ1 is linked to Alzheimer disease.