This may arise as a consequence of how CSCs react to NK cell IFNγ efflux [Liu et al., 2018], especially to IFNγ-induced IDO and kynurenine, which upon release activates the AhR on NK cells and other cells in the emerging tumour microenvironment, thereby initiating a pattern of CSC influence on acetyl-CoA, the melatonergic pathway and metabolism in other cells. The gene discussed is IDO1; the disease is neoplasm.