In EGFR-mutated NSCLC models, tumor cells that survive treatment with an EGFR inhibitor are synthetically dependent on ATM in the DDR pathway, and combined treatment with an ATM kinase inhibitor eradicates these cells in vivo.35 In the present study, our analysis suggests that sotorasib-induced apoptosis is protected by the activation of the WEE1-CHK2 axis in KRAS-mutated cancer cells (Figure 6G). This evidence concerns the gene EGFR and neoplasm.