These observations are consistent with earlier reports that IDO1-mediated tryptophan depletion is a key mechanism of IFNγ-dependent tumor cell growth inhibition, an effect which has recently emerged as a potential contributor to the failure of IDO1 inhibitor clinical trials.27–34 Additionally, the pan-caspase inhibitor Q-VD-OPh (QVD), but not the ferroptosis inhibitor ferrostatin-1, partially protected A375 cells against CTLlow and IFNγ exposure, implicating caspase-dependent apoptosis but not ferroptosis in CTLlow- and IFNγ-induced initial cancer cell death (Figure S1M). The gene discussed is IFNG; the disease is neoplasm.