For example, MET pathway-targeted anticancer therapies might be effective in PDACs in which MET mutations are present, to additionally target EMT-like tumour budding.66 As mutations in the receptor tyrosine kinases MET and ERBB2 can be present simultaneously in a small number of PDACs,67 dual MET and ERBB inhibition, which has been shown to overcome intratumoural plasticity in osimertinib-resistant advanced non-small-cell lung cancer, could also be exploited in pancreatic cancer.52 Here, MET is linked to familial pancreatic carcinoma.