By investigating the mechanism of drug action, we found that extinction of Met oncogenic signaling by Triflorcas occurs through at least three distinct mechanisms: a) by restraining Met activity [19], its phosphorylation, and phosphorylation of its immediate downstream signals such as Gab1; b) by enhancing Met internalization and degradation; c) by decreasing the phosphorylation levels of Akt and of its downstream targets mTOR, p70S6K, and S6 ribosomal protein, one pathway known to ensure Met dependency of cancer cells [22]. This evidence concerns the gene MET and cancer.