Background:The theory of intersystemic reorganization, along with the ability of people with chronic aphasia to recover language function, suggests that a high-tech augmentative and alternative communication (AAC) device could be employed as a dual-purpose tool that simultaneously facilitates language recovery and compensates for deficits. To date, treatments based on intersystemic reorganization have focused on writing, drawing, and gesturing. Further, despite a movement to identify neural mechanisms that support intervention-related recovery, the neurobiological markers of AAC-induced changes have not been established. Aims: The purpose of this study is twofold: (1) to examine the feasibility of providing a high-tech AAC treatment to people with chronic aphasia, with the goal of evoking changes in spoken language; and (2) to identify evidence of AAC-induced changes in brain activation. Method and Procedures: We employed a pre- and post-treatment design with a control (usual care) group to observe the impact of an AAC treatment on aphasia severity and spoken discourse. Further, we used functional magnetic resonance imaging (fMRI) to examine associated neural reorganization. Outcomes and Results: Compared to the usual care group, the AAC intervention trended toward larger treatment effects and resulted in a higher number of responders on behavioral outcomes. Both groups demonstrated a trend toward greater leftward lateralization of language functions via fMRI. Secondary analyses of responders to treatment revealed increased activation in visual processing regions, primarily for the AAC group. Conclusions: This study provides preliminary guidance regarding how to implement AAC treatment in a manner that simultaneously facilitates language recovery across a variety of aphasia types and severity levels while compensating for residual deficits in people with chronic aphasia. Further, this work motivates continued efforts to unveil the role of AAC-based interventions in the aphasia recovery process and provides insight regarding the neurobiological mechanisms supporting AAC-induced language changes.