Despite these and other unknowns, the recent data by Beziaud et al. raise the intriguing possibility that the detrimental effects of indolent type I IFN signaling on tumor progression and sensitivity to treatment [5, 6] may involve, at least in part, IFNγ-dependent immunoediting and the resulting selection of aggressive CSCs (Fig. 1). The gene discussed is IFNG; the disease is neoplasm.