In the DLBCL cells, HDAC1,2 via their interaction with PRC2 containing the hyperactive EZH2 maintain an aberrant ‘H3K27me3>H3K27ac’ state, which likely promotes the lymphomagenesis and/or survival of these lymphoma cells, through repressing the DNA damage response genes. The gene discussed is HDAC1; the disease is diffuse large B-cell lymphoma.