LAG3 and neoplasm: Contributing mechanisms include upregulation of compensatory inhibitory checkpoints such as T-cell immunoglobulin and mucin-domain containing-3 (TIM-3), lymphocyte-activation gene-3 (LAG-3) and T-cell immunoreceptor with Ig and ITIM domains (TIGIT) (93–95), disruption of antigen-presentation machinery through loss of MHC-I or β2-microglobulin (96, 97), and expansion of immunosuppressive cellular subsets, including tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs) (98).