In normal cells, the transcriptional activation occurs rapidly in response to cytokine signaling and is transient, whereas oncogenes with tyrosine kinase activity, e.g., c-Src and activated members of epidermal growth factor receptor family, keep STAT3 constitutively active in many cancers.27–29 For a long time, it has been assumed that STAT3-mediated promotion of tumor growth depends entirely on its well-described transcriptional activities. This evidence concerns the gene STAT3 and cancer.