Importantly, exhausted T cells demonstrate upregulation of multiple inhibitory receptors/immune checkpoints that bind to their ligands expressed by tumor cells (Figure 1), antigen-presenting cells (APCs) and myeloid-derived suppressor cells (MDSCs) in TME, such as programmed death 1 (PD-1), cytotoxic T lymphocyte antigen 4 (CTLA-4), lymphocyte activation gene 3 protein (LAG-3), T cell immunoglobulin domain and mucin domain-containing protein 3 (TIM-3), and TIGIT (T cell immunoreceptor with Ig and ITIM domains) [11–14]. This evidence concerns the gene CTLA4 and neoplasm.