E2F1 and cancer: By using E2F1 WT and Cr cells, combined with chemical inhibition of PRMT5 activity, we established unequivocally that E2F1 is crucial for PRMT5 to retain cancer cells in the proliferative state; thus, inactivating PRMT5 in E2F1 WT cells prompted increased levels of the sub-G1 fraction, highlighting a growth-promoting role for PRMT5 mediated by E2F1.