Treatment of EGFR mutant NSCLC, ALK rearranged NSCLC, KRAS (Kirsten rat sarcoma viral oncogene homolog) mutant NSCLC, BRAF mutant melanoma, FLT3 (fms-like tyrosine kinase 3) mutant acute myeloid leukemia (AML), and KRAS mutant pancreatic ductal adenocarcinoma cell lines with increasing doses of their cognate targeted therapies for 24h led to increased amounts of autophosphorylated ATM at serine residue 1981 (S1981), a site required for activation of the downstream DNA damage response pathway, and γ-H2AX, a canonical marker of DSBs (Fig. 1A and fig. This evidence concerns the gene ALK and pancreatic ductal adenocarcinoma.