Although both vorinostat and DMC-HA are inert to HDAC4 and HDAC5, it has been reported that class IIa (including HDACs 4, 5, 7, and 9) enzymes are inefficient on histone substrates; class I HDACs, especially HDACs 1–3, and HDAC 6 (class IIb) are considered key targets for cancer treatment (29). This evidence concerns the gene HDAC5 and cancer.