STAT3 and gastric cancer: Although suppression of IL-6 dependent- or independent expression of other STAT3-responsive reporter expression by cirsiliol in Hep3B cells or by carnosol in HCT116 cells, respectively [3,4], and luteolin-dependent inhibition of STAT3 activation through disruption of binding of HSP90 to STAT3 in gastric cancer cells have been reported [5], suppression of IL-6-dependent expression of the IL-6 responsive reporter expression and change in the quantity of phosphorylated or total STAT3 proteins by these three compounds simultaneously have not been compared in HepG2 cells.