Increased arginase activity may stimulate tumor growth via different mechanisms including a reduction in NO-mediated tumor cytotoxicity [283], increased cellular proliferation due to modified polyamine and proline synthesis, deregulation of the T cell receptor (TCR) signaling, and subsequent unresponsiveness of CD8+ T cell [284], and an increased ability of myeloid suppressor cells to inhibit proliferation of T cells [285]. Here, CD8A is linked to neoplasm.