Notably, we exogenously overexpressed wild-type E2F7 or E2F7-Adel mutant in NPC cells with VIRMA silenced, and found that overexpression of wild-type E2F7 could rescue the cell proliferation, migration, and invasion defects by VIRMA depletion, whereas the E2F7-Adel mutant could not (Fig. S4, F–I). Here, E2F7 is linked to nasopharyngeal carcinoma.