Next, we used the nonmetabolizable glucose analog 2-DG and the Hsp90 inhibitor 17-AAG, a derivative of geldanamycin (GA) which had been reported to not only destabilizes the HIF-1α protein but also disrupts STAT3- HIF-1α activation axis [37, 38], along with IMQ co-treatment in cancer cells and xenograft tumor mouse models to test this hypothesis. This evidence concerns the gene STAT3 and neoplasm.