Various reports from the cancer field suspect that Class I HDAC activity and increased deacetylation of STAT3 appear to be required for its phosphorylation at Tyr705 and nuclear translocation as HDAC1, -2 and -3 have been reported to reduce STAT3 acetylation [261,262] and as selective inhibition of Class I HDACs was sufficient in efficiently suppressing STAT3-pTyr705 phosphorylation and its signalling in a variety of malignant cells [262,263,264]. Here, STAT3 is linked to cancer.