The key function of K-Ras in this interaction is also supported by the enhanced sensitivity of KRAS-mutant lung cancer cells to MEK inhibition after ATM loss [76] and radiosensitization of KRAS-mutated pancreatic cancer cells after MEK targeting through inhibition of HR- and NHEJ-dependent DSB repair [77]. This evidence concerns the gene MAP2K7 and pancreatic neoplasm.