PDCD1 and neoplasm: Targeting LAG-3 in combination with other checkpoints to enhance antitumor immunity is a rational approach as LAG-3 has often been found co-expressed with PD-1 on tumor-infiltrating T cells in murine models (13–15) and human disease (16–18), and persistent upregulation of both is connected to a state of T cell dysfunction termed exhaustion in models of chronic viral infection (19).