Mechanistically, we have demonstrated Hdac7 can directly interact with Stat3 and deacetylate Stat3 proteins, and decreasing Hdac7 expression by mutation in mice or shRNA in human lung cancer cells results in enhanced acetylation and phosphorylation of Stat3 without significant effect on the expression of JAK1 and AKAP12 (Additional file 1: Figure S1B). The gene discussed is HDAC7; the disease is lung cancer.