These studies thoughtfully suggest that upregulation of the ATR-Chk1 axis is efficient for tolerance to oncogenic RAS-induced RS, while suppressing DDR-mediated cell death, which is a barrier to tumorigenesis, highlighting the dosage-dependent dual function of ATR modules, on one hand as a barrier for tumor development and on the other hand as a supporter of cell survival in response to oncogenic-RAS activation during cancer progression (Figure 1). Here, CHEK1 is linked to neoplasm.