The Mesenchymal Epithelial Transition (MET) proto-oncogene encodes the MET receptor tyrosine kinase, also called c-MET or hepatocyte growth factor (HGF) receptor. MET is a ubiquitously expressed cell surface receptor that leads to the activation of several downstream intracellular pathways which promote cellular growth and proliferation, motility, migration and angiogenesis. Dysregulation of MET via gene amplification, germline or somatic mutations or receptor overexpression has been observed in a variety of epithelial cancers, including breast prostate cancer, non-small cell lung cancer, renal papillary carcinoma, hepatocellular and gastric carcinomas. Genetic alterations in MET have been identified in 0.4% of thyroid carcinomas. The prognostic and predictive significance of MET mutations in thyroid cancer is not clear and correlation with other clinical and laboratory findings is necessary. M362T has been identified in the scientific literature, but has not been biochemically characterized and therefore, its effect on protein function is unknown. This variant is reported as a benign/likely benign germline variant in ClinVar (https://preview.ncbi.nlm.nih.gov/clinvar/variation/93565).