Together, these results reveal that intrinsic PD-L1 signaling can account for some of the IFN-regulated PTIS observed in in vivo-derived resistance models, but these secretory changes were partial and not consistent (Fig. 5I,J show PTIS summary: Fig. EV4G show statistics summary for all in vitro studies) indicating that tumor:immune cell interactions play a key role in PTIS adaptations in treatment-sensitive tumors. The gene discussed is IFNA1; the disease is neoplasm.