This is clearly exemplified in the gp130757F/F mouse model of gastric cancer development, in which a Phe for Tyr substitution at the 757 position on the intracellular arm of the IL-6 family signalling receptor gp130 simultaneously prevents SHP2 and SOCS3 binding, resulting in inhibition of ras/MAP kinase signal transduction, and hyperactivation of STAT3 by constitutive phosphorylation [23], [24], [26]. This evidence concerns the gene STAT3 and gastric cancer.