However, in NSCLC cancers spreading to the brain, several mechanisms have been observed that are potentially involved with organ-tropism, such as the epithelial–mesenchymal transition mechanism (loss of E-cadherin, overexpression of vimentin and N-cadherin), the activation of migration-related chemokines (high CXCL12 and its receptor CXCR4 levels), and the activation of EGFR/MET/VEGF pathways [31]. Here, MET is linked to non-small cell lung carcinoma.