Since clinically usable STAT3 inhibitors are still under development, STAT3 activated resistant tumor BoC32 C2 was treated in combination with CET and ruxolitinib, a JAK1/2 inhibitor or with the histone deacetylase (HDAC)-inhibitor vorinostat both of which have been shown to cause an inhibitory effect on STAT3 signaling [79, 80]. The gene discussed is HDAC9; the disease is neoplasm.