Given their functional role in both transcriptional regulation and modifications of non-histone substrates, HATs and HDACs have been implicated in many different disease states, including inflammatory diseases due to HAT-mediated post-translational modification of NF-κB, HAT-mediated acetylation of tau and concomitant increased expression of phosphorylated tau in Alzheimer’s disease, as well as overexpression, underexpression, and/or mutation of both HATs and HDACs in many different forms of cancer, as reviewed elsewhere (20, 40, 45–49). This evidence concerns the gene TMPRSS11D and cancer.