T cells can be virally modified to express MHC-independent antibody binding domains on their surface. CD19 directed chimeric antigen receptor T cell (CAR19) therapy is an application of this approach, and has shown significant promise in localizing the immune response against hematological malignancies. Nevertheless, despite the commercial and scientific success of CAR therapies, many patients fail treatment and relapse due to mechanisms of resistance. More specifically, suboptimal CART performance is driven by high expression of immune checkpoint inhibitors such as PD-1, CTLA-4, and TIM-3, which function to inhibit the immune response and prevent lymphocytes from efficiently expanding. As a result, the next frontier for CART therapy involves making genomic changes to primary T cells and modulating checkpoint expression prior to viral transduction. Certain mediators, such as SHP1 and SHP2, play a significant role in decreasing T-cell cytotoxicity and can be knocked out via CRISPR-Cas9 to enhance anti-tumor potential. Therefore, we engineered CAR19 SHP1, SHP2, and Dual (SHP1 and SHP2) KO T cells to evaluate whether decreased SHP expression will lead to more clinically relevant CART therapy. Our results show that CAR19 SHP KO T cells have higher absolute counts, luciferase killing %, and cytokine secretion compared to standard CAR19. Additionally, expansion of CAR19 SHP KO selectively favors CD4+ differentiation, revealing a potential exhaustion-resistant mechanism that is unique to the PD-1/SHP axis. Finally, we conclude that SHP2 has low expression in resting T-cells and may be regulated via an activation-dependent manner. We hope to use these results to inform the next generation of CART development and emphasize the relevance of phosphatase proteins in refractory blood cancers.