Chronic antigen stimulus, accumulation of coinhibitory receptors, and loss of costimulation lead to progressive CD8+ T-cell dysfunction.9 T-cell immunoglobulin and mucin domain-3 (TIM-3) is a coinhibitory receptor expressed on immune effector and myeloid cells.10 Tumor-site expression of TIM-3 correlates with disease progression across cancer types,11 12 while knockdown or silencing of HAVCR2 (encoding and referred to as TIM-3) reinvigorates CD8+ T cells against advanced solid tumors,10 establishing its role as a key immune checkpoint of adaptive immunity. This evidence concerns the gene CD8A and cancer.