In our previous study, VPA, a class I and II HDACi, has been shown to increase the sensitivity of tumor cells to HU treatment; for example, VPA reduced S-phase arrest of the cell cycle and thus has a chemo-sensitizing role in response to HU-induced replication arrest by inhibiting Chk1 signaling [10, 32, 33]. This evidence concerns the gene CHEK1 and neoplasm.