Starting from a mouse model platform with defined senescence-compromising gene defects, primary Eμ-myc transgenic LC, stably overexpressing Bcl2 (as naturally detected at high levels in many lymphomas including DLBCL15) to block drug-induced apoptosis, enter TIS in vitro and in vivo, if senescence-essential gene loci such as Suv39h1 or p53 alleles were not deleted22,25,28 (Fig. 3a, Supplementary Fig. 3a, b). Here, BCL2 is linked to lymphoma.