To test whether these differences were due simply to tissue type, we developed stable resistance in an additional KRAS-mutant pancreatic cancer cell line; indeed, the intersection of differentially expressed genes was no greater among the pancreatic cancer lines (Supplementary Fig. 2a, Supplementary Table 3), nor were the associated gene annotations using GSEA (Fig. S2b, Supplementary Table 4). Here, KRAS is linked to pancreatic neoplasm.