Notably, while enforced PU.1 induction without additional ADR exposure promoted the B-to-M transition as indicated by expanding fractions of CD115+ cells in TIS-capable control;bcl2 cells, no such effect was seen in TIS-incapable Suv39h1-deficient cells, presumably reflecting the absent cooperation of senescence-associated chromatin remodeling with PU.1 action towards myeloid cross-differentiation in the latter, thereby explaining the observed lack of ADR-inducible T-cell immunogenicity in these TIS-incapable lymphomas (Supplementary Fig. 10e). This evidence concerns the gene SPI1 and lymphoma.