Cloning animals by somatic cell nuclear transfer (SCNT) has been successful over the past decade; however, the success rate is still extremely low. In mice, compared with other species, the success rate for the procedure has been particularly low, and most of the inbred mouse strains have never been cloned. Recently, Van Thuan et al. indicated that treatment of SCNT mouse embryos with Scriptaid, a histone deacetylase inhibitor (HDACi), significantly improved the full-term development of mouse clones. To characterize the effect of Scriptaid on the enhancement of embryos’ development after SCNT, we investigated the expression and localization of the protein TIF1β during the preimplantation development of cloned embryos of ICR strain mice. In untreated cloned blastocysts, TIF1β was absent in the inner cell mass (ICM) cells, but it was hyperexpressed in the cytoplasm of trophectoderm (TE) cells; however, the protein was detected in both TE and ICM cells in ICSI-generated blastocysts. Here, we show that the treatment of cloned embryos with Scriptaid induced a normal expression level of TIF1β in the nucleoplasm of 2-cell embryos and ICM cells of blastocysts. The results show that the success rate of embryos in developing to the blastocyst stage via Scriptaid-treated cloning was higher than that of untreated cloned embryos. We suggest that Scriptaid corrected the expression and the location pattern of TIF1β and improved the preimplantation development of cloned ICR mouse embryos.