Chromatin organization and permissive epigenetic landscapes are important in regulating cell identity, persistence, and effector gene expression. However, it remains unclear how chromatin remodelers such as Arid1a, a component of the canonical BAF complex, actively maintains and opens important enhancer regions in cytotoxic lymphocytes. We have previously observed that NK cells undergo rapid and dynamic changes in their accessible chromatin regions during development and activation, and that the most profound changes occur at enhancer rather than promoter regions. Here, we show that NK cells express high levels of Arid1a transcript, and deletion of Arid1a in NK cells reduces cell number and frequency, with an enrichment in immature CD27⁺ CD11b^- NK cells.  Arid1a-deficient NK cells also have impaired expression of many activating and inhibitory receptors, including Ly49H, DNAM-1, and Ly49C/I, suggesting an essential role for Arid1a in regulating NK cell development and maturation. Furthermore, Arid1a-deficient NK cells produce less IFN-g and CD107a when stimulated with plate-bound antigen receptor (NK1.1) or exogenous cytokines (IL-12 plus IL-18). Furthermore, Arid1a-deficient Ly49H⁺ NK cells fail to clonally expand and differentiate in response to MCMV. Together, these studies provide evidence that Arid1a is an essential regulator of NK cell development, homeostasis, and effector function. Understanding how epigenetic regulators govern the immune system is essential towards generating novel NK cell-based immunotherapy strategies against cancer and infectious diseases.