In an attempt to study the clinical significance of the SP1-AURKB-ATM axis in GC development, we utilized an SP1 inhibitor, plicamycin, to suppress SP1 expression in AGS and SGC cells and found that SP1 obviously inhibited the expression levels of AURKB and the levels of phosphorylated ATM and P38, while upregulating the level of phosphorylated P53 (Supplementary Fig. 2d). The gene discussed is ATM; the disease is gastric cancer.