KT-531 wasexamined for its ability to induce acetylation of α-tubulin,a prominent substrate of HDAC6, and histone H3 (HDAC Class I substrate).56 Initially, model cancer cells (HeLa) were subjectedto 6 h incubation with increasing doses of KT-531 or citarinostatand target engagement was analyzed via immunofluorescence assays.In KT-531-treated cells, significant acetylation of α-tubulinwas observed, with no observable change in acetylation of histoneH3 (Figure 3a,b). This evidence concerns the gene HDAC6 and cancer.