Various reports from the cancer field suspect, that increased deacetylation of STAT3 seems to be required for its phosphorylation and nuclear translocation, as various specific class I and class II-HDAC inhibitors (valproic acid, entinostat, romidepsin, ‘mercaptoacetamid-based HDACi W2’) as well as the pan-HDAC inhibitor LBH589 were shown to suppress STAT3-phosphorylation/activation in a variety of malignant cancers, and which was associated with significantly reduced migration and invasiveness of cancer cells [71–74]. The gene discussed is STAT3; the disease is cancer.