Wang et al. (2017) performed a genome-wide screening in KRAS-mutated pancreatic adenocarcinoma to investigate RTK-RAS-MAPK pathway reactivation and found that gene ATXN1L deletion caused a decrease in protein CIC (capicua transcriptional repressor), leading to increased cellular resistance, and determined the ATXN1L-CIC-ETS transcription factor axis to be a mediator of resistance to MAPK inhibitors. The ERN1-JNK-JUN pathway is present in KRAS mutant colorectal cancers and is involved in regulating MEK inhibitor resistance in colon cancer (Šuštić et al., 2018). Here, CIC is linked to pancreatic adenocarcinoma.