Based on previous findings showing therapy-induced tumor repopulation via soluble factors 13, increase in IL6 expression through the RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways 36, 37, and Hsp90 blockade-caused secretion of IL6 35, 38, a ligand for IL6 receptor that activates STAT3, we speculated that activation of RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways after 17-AAG treatment caused transcriptional changes in IL6 expression, leading to STAT3 activation. The gene discussed is STAT3; the disease is neoplasm.