To study the role of Chk1 in mediating CIP2A upregulation in neurons, and to explore whether upregulated Chk1-CIP2A signaling induce AD-like pathogenesis, we treated primary neurons with Aβ oligomers (2 μM) for 48 h, with or without pre-incubation of Chk1 inhibitor SB218078 (1 μM) or PF477736 (1 μM) for 48 h. This evidence concerns the gene CHEK1 and Alzheimer disease.