While inhibition of Shp2 had little effect on pAkt and pStat3 in our mouse model, it is possible but remains to be tested that combining Shp2 inhibition with blockage of the phosphoinoside-3-kinase-Akt pathway and/or Stat3 signaling may be a more effective therapy for EGFR mutant-associated NSCLC that develop resistance to the first-line EGFR PTK inhibitor therapy. This evidence concerns the gene STAT3 and non-small cell lung carcinoma.