In sharp contrast to the prevailing model, we had previously performed kinetic analyses from highly synchronized normal cells and p16-deficient tumor cells, and found that cyclin D:Cdk4/6 was constitutively active throughout all of the early G1 phase at the same time points that Rb was actively binding E2Fs and repressing E2F target gene expression (Ezhevsky et al., 1997, 2001; Haberichter et al., 2007). The gene discussed is RB1; the disease is neoplasm.