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Met is a receptor protein-tyrosine kinase (RPTK) for hepatocyte growth factor (HGF), which is a multifunctional cytokine controlling cell growth, morphogenesis, and motility. Met overexpression has been identified in a variety of human cancers (1). Met kinase domain possesses unique features that distinguish met from other members of the src family of protein tyrosine kinases. These results also demonstrate that the product of the activated met gene is a fusion protein and that the amino terminal end of this fusion protein exhibits homology to laminin B1 (2). Data suggest that RanBP9, functioning as an adaptor protein for the Met tyrosine kinase domain, can augment the HGF-Met signaling pathway and that RanBP9 overexpression may cause constitutive activation of the Ras signaling pathway (1). Hereditary papillary renal carcinoma (HPRC) is a recently recognized form of inherited kidney cancer Results suggest that missense mutations located in the MET proto-oncogene lead to constitutive activation of the Met protein and papillary renal carcinomas (3)