The product of the retinoblastoma (RB) susceptibility locus suppresses neoplastic growth and exists as a family of differentially phosphorylated, DNA binding proteins. The unphosphorylated member(s) of this group can interact specifically with the transforming product of the SV40 genome, large T antigen (T). The genetics of this interaction further suggest that T-RB complex formation is an important step in the mechanism of T function as a transforming element and that T may operate in this regard by perturbing one or more aspects of the RB growth suppression function. Results of various analyses of the details of complex formation suggest at least one generic function for RB, contributing to the regulation of the G1/S transition in the mammalian cell cycle.