Still, it has been shown that Rb/E2F-1 interaction can be inhibited by Mdm2, whose expression is increased by p53 when methylated by SETD7 [41], once again supporting a positive role of SETD7 on cell cycle progression through E2F-1, at least in p53 wild-type tumours (Figure 9). Here, E2F1 is linked to neoplasm.