119). Additionally, altered 3-HAA concentrations promote the activation of T and NK cells by increasing the expression of CXCL11 and KLRD1 (Ref. 120). IDO in thyroid cancer cells produces Kyn, which leads to NK cells dysfunction by a possible mechanism that reduces NK cells function through the signal transduction and transcriptional activator STAT1 and STAT3 pathways (Ref. 121). Furthermore, the AhR-IDO axis, modulated by both acute and long-term endurance exercise, plays a role in controlling NK cell activity and contributing to immunological modulation (Ref. 122). This evidence concerns the gene IDO1 and thyroid cancer.