To gauge the efficacy of combining AURKA and EGFR inhibition in KRASmut lung cancers with wt EGFR, we first confirmed their protein expression in a panel of eight cell lines, including six lung cancer with driver mutations in KRAS, NRAS, and EML4-ALK, one lung cancer (H322M) with a homozygous mutation in TP53 proposed to have a driver function (38), and a fibroblast control line (FC1010; Table 1; Fig. 2A). This evidence concerns the gene KRAS and lung carcinoma.