Overall, two compatible theories can explain the observed results: first, E2F1-R166H decreases apoptosis and its abrogated cell cycle role is compensated for by other members of its family; and second, heterozygous E2F1-R166H behaves like SV-40 large T antigen, interfering with the tumor suppressive role of Rb and allowing its wild-type counterpart to drive cell division. This evidence concerns the gene RB1 and neoplasm.