STAT3 and cancer: STAT3 activity is increased in ~50% of all cancers [10], due, in many instances, to activation of signaling molecules upstream of STAT3, including receptor tyrosine kinases (RTK; e.g. epidermal growth factor receptor, EGFR), tyrosine kinase-associated receptors (e.g. the family of IL-6 cytokine receptors or G-protein coupled receptors, GPCR) [11, 12], and Src kinases (e.g. Src, Lck, Hck, Lyn, Fyn, or Fgr) [12, 13].