STAT3 and non-small cell lung carcinoma: A newly discovered heat shock protein 90 (Hsp90) inhibitor, NCT-80, bound directly to the C-terminal ATP-binding pocket of Hsp90, disrupted the interaction between Hsp90 and STAT3, and degraded the STAT3 protein, thereby reducing CSC-like phenotypes of NSCLC cells and their sublines with acquired resistance to anti-cancer drugs [71].