Results from chromatin accessibility analysis in lung adenocarcinoma cells from a genetically engineered mouse model (GEMM) of Kras LSL-G12D/+ and Trp53 fl/fl (KP) initiated with BRG1 showed that metastasis-derived tumor cells were enriched for peaks with AP-1 transcription factor motifs, while other tumor cells were depleted of AP-1 peaks, suggesting that AP-1 may be involved in the metastasis of the tumor [66]. This evidence concerns the gene JUN and lung adenocarcinoma.