Since anti-HDAC therapies are non-selective and target epigenetic alterations [17] and anti-EGFR therapies such as erlotinib have failed to show clinically meaningful benefit in PDAC [18,19], we chose to investigate MET, which is a promising therapeutic target for various cancers and is overexpressed, upregulated, and inversely associated with prognosis in PDAC [9,10,11]. This evidence concerns the gene MET and cancer.