Our results align with these previous studies suggesting that PD-L1 has both activating and inhibitory domains that cross-talk with IFN signaling where tumor cells following genetic and in vitro therapeutic PD-L1 disruption can recapitulate some; but not all, of the IFN-regulated PTIS observed after PD-L1 resistance (Gato-Canas et al, 2017). The gene discussed is IFNA1; the disease is neoplasm.