Recent studies revealed that SETD7 can methylate the K873 of pRB, thereby increasing RB1-HP1 interactions, which in turn inhibits transcription 20; methylate DNMT1 at K142 and enhance proteasome-mediated DNMT1 degradation to exert cancer suppressive activity 21; methylate SUV39H1 at K105/123 to inhibit SUV39H1 methyltransferase activity in response to DNA damage, thereby inducing genomic instability and inhibiting cell proliferation 22. The gene discussed is RB1; the disease is cancer.