KRAS and pancreatic adenocarcinoma: 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).