Recent studies on dysfunctional tumor-specific or exhausted CD8+ T cells have shown that epigenetic changes in chromatin accessibility or methylation can maintain such states (Ghoneim et al., 2017; Pauken et al., 2016; Philip et al., 2017), which is one potential explanation for the cell-intrinsic nature of the tolerance seen in our model. The gene discussed is CD8A; the disease is neoplasm.