In this study, we showed the emergence of 17-AAG resistance in NSCLC cells through compensatory activation of Akt- and ERK-mediated sequential events; this includes the transcriptional upregulation of IL6 and subsequent activation of STAT3, which in turn stimulates transcription of Wnt ligands and activation of Wnt signaling pathway. Here, STAT3 is linked to non-small cell lung carcinoma.