The tyrosine kinase MET and the WNT/β-catenin signaling pathway (WNT signaling) have both received considerable interest as targets in cancer therapy due their involvement in carcinogenesis.1–3 MET is dysregulated in a wide range of malignancies, and is correlated with a poor prognosis.4 WNT signaling is critical for cell repair and stem cell maintenance, and aberrant activity is closely associated with the development and growth of a plethora of cancerous diseases. This evidence concerns the gene MET and cancer.