Stable transfer of LSD1 and JMJD2C genes into control;bcl2 lymphomas, similar to inactivation of Suv39h1, resulted in sharply reduced levels of the H3K9me3 mark and the senescence-associated cyclin-dependent kinase inhibitor p16INK4a by immunoblot analysis, and impaired ADR-induced senescence in vitro, while leaving drug-induced DNA damage response signaling via γ-H2AX and serine-18-phosphorylated p53 (p53-P-Ser18) intact (Fig. 4a, Supplementary Fig. 4a), resulting in demethylase-unaffected apoptotic death in non-Bcl2-protected lymphomas (Supplementary Fig. 4b). This evidence concerns the gene H2AX and lymphoma.