Overall, the interactions of the AhR with regulators of PDC-regulated acetyl-CoA provides a metabolic framework that integrates wider bodies of data pertaining to the induction of ‘exhaustion’ in CD8+ T cells and NK cells in the tumour microenvironment, with effects mediated via alterations in the dynamic metabolic interactions of tumour microenvironment cells, with key metabolic processes indicated in Figure 1. This evidence concerns the gene PDC and neoplasm.