Chimeric Antigen Receptor (CAR) T-cell therapy is a type of immunotherapy which involves engineering a patient’s T-cells to present receptors specific to their cancerous cells. Anti-CD19 CAR T-cell therapy has proven very successful in patients with relapsed B-Cell Acute Lymphoblastic Leukemia (B-ALL). Unfortunately, a significant portion of patients experience CD19+ relapse due to premature CAR T-cell extinction. This phenomenon is not accurately described in current models; most describe it as a result of a prey-predator relationship between CAR T-cells and leukemic cells, even though CD19+ relapses occur exclusively in the absence of CAR T-cells. Therefore, we propose a new mechanism which can explain CD19+ relapse in the absence of CAR T-cells – the stimulation of T-regulatory cells by leukemic cells. T-regulatory cells moderate immune responses by inactivating effector T-cells. Surprisingly, they account for a larger proportion of T-cells than usual in tumor microenvironments, likely because cancerous cell secrete Transforming Growth Factor (TGF) beta, a protein which stimulates conversion of T-cells into T-regulatory cells. Working from existing ordinary differential equation models of anti-CD19 CAR T-cell therapy and B-ALL, we develop a model which includes T-regulatory cells and TGF – beta. We demonstrate that the conversion of CAR T-cells by TGF – beta combined with the inactivation of CAR T-cells by T-regulatory cells can explain CD19+ relapse in the absence of CAR T-cells.