Given that (1) STAT3 is consistently found to be hyper-activated in CRC; (2) STAT3 pro-tumorigenic properties are commonly mediated through EGF, IL-6 and IL-11 ligand/receptor systems in CRC; (3) STAT3 is often re-activated through uninhibited ligand/receptor systems; and (4) a successful anti-STAT3 agent has yet to be approved in any cancer setting, we explored the possibility of identifying agents currently approved for other indications that may also display novel anti-STAT3 activity. This evidence concerns the gene IL11 and cancer.