Rab5 preserves CAR-T function after repeated tumor contact. Repeated tumor contact leaves molecular residue on CAR-T cells through bidirectional trogocytosis. Tumor antigens are transferred onto the CAR-T cell surface, while CAR molecules can also be captured by tumor cells. When Rab5 is low, CAR-T cells fail to adequately clear this acquired antigen via Rab5-mediated endocytosis, leading to accumulation of surface antigen, loss of available CAR, and increased fratricide. By contrast, restoration of Rab5 improves handling of these postcontact consequences by promoting clearance of trogocytosed antigen and recycling of functional CAR back to the cell surface. In this way, Rab5 helps maintain a usable receptor landscape on CAR-T cells and supports more sustained tumor killing after repeated tumor encounters.