AKT represents one of the most important proteins that is adaptively regulated in relation to cancer cell survival, and increased phospho-AKT (P-AKT) is thought to contribute to an apoptotic resistance phenotype.14, 15, 16 HDAC6 inhibition by C1A (increased acetyl α-tubulin with no change in acetyl H3) was found to be associated with a time-dependent increase of P-AKT (Figure 1a). This evidence concerns the gene HDAC6 and cancer.