In this study, our results suggested that 2,4-DAQ inhibited the viability and clonogenicity of gastric cancer cell lines (AGS and MKN45) in a dose-dependent manner and promoted the apoptosis of AGS and MKN45 cells, which can be verified by the presence of apoptotic markers (caspase activation and cleavage of PARP-1). Here, PARP1 is linked to gastric cancer.