CD8+ T cell memory is pivotal for long-term protective immunity, but often impaired in the tumor setting, partially due to extensive T cell exhaustion and loss of memory precursors, which is not reversed by checkpoint blockade immunotherapy. It is, however, incompletely understood how T cell exhaustion is maintained, which in turn impedes functional CD8 memory development. Here we report that mice with CD8+ T cell-restricted deficiency of Neuropilin 1 (NRP1) showed significantly enhanced protection from re-challenged B16.F10 tumors, despite unchanged primary tumor growth. NRP1 acted on multiple inhibitory receptors (IRs)-expressing CD8+ T cells to reinforce their exhaustion status and restrain the potential of memory differentiation, by repressing the Id3-dependent transcription program. These data reveal NRP1 as a unique “immune checkpoint” contributing to the lineage stability and blocking the memory conversion in the exhausted CD8+ T cells, a mechanism of action that is distinct from that of well-known immune checkpoints (PD1, CTLA4, LAG3). Blockade of checkpoint inhibitors of T cell memory may be necessary to achieve durable anti-tumor immunity.