MET and cancer: When some of these alternatives derived in a truncated MET receptor, it shows a constitutive expression because the loss of the Tyr1003 residue located in the JMD prevents the binding of the E3 ubiquitin ligase Cbl and proteasomal degradation, which have shown overactive MET signaling pathways, triggering an exacerbate cell proliferation and invasion, contributing to the evolution of cancer and bad prognosis [19,20].