Therefore, Wu et al. established a model in which the tumor-suppressive actions of ARID1A involve two inhibitory mechanisms of CDC25C function: (1) negative regulation of the upstream activator (AURKA-PLK1 axis) of CDC25C at the transcriptional level and (2) positive regulation of the upstream inhibitor (ATR-CHK1 axis) of CDC25C at the posttranslational level. This evidence concerns the gene ARID1A and neoplasm.