In patients with CRC, research within the center concerning drug‐resistant signaling pathways implicated activation of c‐MET as a key mediator of resistance to MEK inhibition in patients with KRAS‐mutant CRC,27 providing the rationale for a successful €6‐million (approximately $6.65 million) European Commission Framework VII‐funded bid for the CCRCB to lead a pan‐European translational clinical trial program with 13 partners from 7 European countries (MErCuRIC trial) (mercuric.eu/). This evidence concerns the gene MET and colorectal carcinoma.