Consistently, ERK/JNK signaling was more significantly activated, resulting in lower DNA damage in response to the chemotherapeutic drug in KRAS-mutant NSCLC cell lines, including NCI-H23, NCI-H2122, NCI-H1573, and NCI-H2009 as compared with KRAS WT lung cancer cell lines such as NCI-H522 and NCI-H292 (Figure 1B). The gene discussed is KRAS; the disease is non-small cell lung carcinoma.