The fact that ATXN3 targeted deletion largely diminished both IFN-γ– and hypoxia-induced PD-L1 expression implies that ATXN3 plays a critical role in promoting PD-L1 expression in inflammatory and hypoxic tumor microenvironment and suggests that ATXN3 regulation of PD-L1 is controlled by extracellular stimuli through distinct pathways. The gene discussed is IFNG; the disease is neoplasm.