Herein, we report the exploitation of well-characterized adaptor-specific RTK docking variants derived from the oncogenic Met receptor, Tpr-Met [8,9,15,16,20], with shRNA and pharmacological interference approaches to define, for the first time, the cancer properties associated with early neoplastic transformation of IECs, induced upon oncogenic mediated activation of either Grb2 or Shc signaling. The gene discussed is SHC1; the disease is cancer.