Taken together, our data suggest that the activity of downstream KRAS pathway target genes, in particular those involved in regulating proliferative and metastatic behaviour, are regulated by MET receptor activity in splice mutant tumours in addition to being overexpressed relative to tumours with only MET amplification, a result that could be due to an apparent bias towards RAS-MAPK pathway activation in METΔex14-expressing cells. Here, KRAS is linked to neoplasm.