Here, we have not only shown that tumorigenesis was inhibited in Hdac7+/−/K-Ras mice and Stat3 was more activated (more phosphorylation of Y705) in Hdac7+/−/K-Ras tumors, but we also demonstrated that suppression of endogenous Stat3 activity in lung tumor cells, by expressing dnStat3, reversed Hdac7 mutant-mediated reduction of tumor number and burden in Hdac7+/−/K-Ras mice. The gene discussed is STAT3; the disease is neoplasm.