The overall findings are summarized in Figure 6G, showing that in the NSCLC case in which KRAS-G12C and TP53 mutations co-exist, sotorasib treatment suppressed ERK, leading to the expression of BIM, which triggered caspase activation through DNA double-strand breaks, whereas WEE1 inhibition reduced the DDR pathway by suppressing CHK2. Here, TP53 is linked to non-small cell lung carcinoma.