Given that ATR promotes RST mediated by PrimPol-dependent repriming to maintain fork speed and ensure cell survival with acquisition of genomic instability in response to KRASG12V-induced RS, we examined whether combined overexpression of PrimPol and ATR could impact OS in KRAS-driven cancer in the same cohort of LUAD patients (shown in Fig. 1a). This evidence concerns the gene KRAS and cancer.