To test this hypothesis, we performed RNA sequencing in parallel with chromatin immunoprecipitation-DNA sequencing (ChIP-seq) for acetylated histone 3, lysine 27 (H3K27ac) in the same treatment-naïve KRAS-mutant pancreatic cancer cell line, as well as at one week of dual-mechanism ERK inhibition and following the development of stable resistance. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.