Heterozygous mutations in the histone acetyltransferase gene KAT6B (MYST4/MORF/QKF) cause cognitive disorders. Congruently, KAT6B is required for brain development, neural stem cell self-renewal and neuronal differentiation in mice. Despite the clear requirement for KAT6B in brain development, its molecular roles remain unexplored. Here we use ATAC sequencing to determine the effects of loss or gain of KAT6B on DNA accessiblity. Overall design: Kat6b knock-out mice were constructed on the C57BL/6 background. Transgenic Tg(Kat6b) mice that overexpress Kat6b were also constructed and maintained on a FVBxBALB/c hybrid genetic background. The mixed genetic background was chosen because Tg(Kat6b) mice are not viable on the C57BL/6 background. Neural stem and progenitor cells were isolated from the dorsal telencephalon of E12.5 mouse embryos and ATAC-seq profiles were constructed. Samples were taken from four Kat6b–/– knockout embryos and four Kat6b+/+ wild-type embryos on the C57BL/6 background, as well as from four Tg(Kat6b) transgenic embryos and four Kat6b wild-type embryos on the FVBxBALB/c genetic background. All samples were also spiked with a fixed amount of DNA from Drosophila S2 cells to aid with normalization.