Loss of the Arabidopsis NFX1-LIKE2 (NFXL2) gene (At5g05660) results in elevated ABA levels, elevated hydrogen peroxide levels, reduced stomatal aperture, and enhanced drought stress tolerance. Introduction of the NFXL2–78 isoform into the nfxl2–1 mutant is largely sufficient for complementation of the phenotype. We show here that cuticular properties are altered in the nfxl2–1 mutant. The NFXL2–78 protein binds to the SHINE1 (SHN1), SHN2, SHN3, and BODYGUARD1 (BDG1) promoters and mediates weaker expression of these genes. The SHN AP2 domain transcription factors influence cuticle properties. Stronger SHN1, SHN2, and SHN3 expression in the nfxl2–1 mutant may cause altered cuticle properties including reduced stomatal density, and partly explain the enhanced drought stress tolerance. The BDG1 protein also controls cuticle development and is essential for osmotic stress regulation of ABA biosynthesis. Stronger BDG1 expression in nfxl2–1 plants may allow elevated ABA accumulation under drought stress. We conclude that the NFXL2–78 protein is part of a regulatory network that integrates the biosynthesis and action of ABA, ROS, and cuticle components.