B-catenin and cyclin D1 have attracted considerable attention due to their proto-oncogenic roles in human cancer. The finding of cyclin D1 as a direct target gene of b-catenin in colon cancer cells led to the assumption that cyclin D1 upregulation is pivotal to b-catenin's oncogenicity. Our recent paper shows that this is not the case; cyclin D1 dampens the oncogenicity of activated b-catenin (MMTV-DN89b-catenin). The relationships and dependencies of b-catenin and cyclin D1 point to distinct, essential and sequential roles during alveologenisis. These results support the concept that both b-catenin's and cyclin D1's actions are more sophisticated than simple acceleration of the cell cycle clock. These proteins are employed at critical junctures involving cell fate decisions that we speculate require specific types of cel cycle to traverse.