KLF5 exerts opposing functions in cell proliferation and tumor growth in prostate epithelial cells, and its acetylation status regulated by TGF-β and likely other signaling molecules28–31 is the determinant, with deacetylation of KLF5 at lysine 369 (K369) promoting tumor growth31 by altering the transcriptional complex of KLF5 in the expression of its downstream target genes such as CDKN2B, MYC, PDGFA, and CDKN1A30,32,33. The gene discussed is MYC; the disease is neoplasm.