We also tested whether PU.1 induction might drive expression of those immune modulators, and found elevated CD86 and PD-L1 expression in human Karpas-422 DLBCL cells upon 4-OHT-enforced PU.1 expression in the absence of ADR, thereby positioning PU.1 downstream or independent of senescence-associated priming of these target gene promoters (Supplementary Fig. 9c). The gene discussed is SPI1; the disease is diffuse large B-cell lymphoma.