Most interestingly, the expression of SOCS2 dose dependently reduced the interaction between IGF1R and STAT3 or STAT5, indicating that SOCS2 acts as a STAT3/STAT5 inhibitor that can competitively bind to IGF1R and thus can attenuate the IGF1-induced STAT3/STAT5 activity in lung adenocarcinoma cells. Here, STAT3 is linked to lung adenocarcinoma.