Start. The CDC28 step was the first step in the cell cycle. From it branched the two pathways of gene activity leading to the cell surface events, budding and cytokinesis, and the nuclear events, spindle pole duplication, separation and elongation, and DNA replication and nuclear division. It was also the step where growth was integrated with division. CDC28 is not executed until the cell reaches a specific size but once the CDC28 event was completed the cell could finish the rest of the cycle without appreciable growth. CDC28 was also the step at which mating was coordinated with the cell cycle. Both pheromones arrested cells at a position, interdependent with the CDC28 step so that when the two cells fused in G1 they were synchronized at the unduplicated spindle pole body stage. Thus CDC28 was of central importance. We called the event that was performed by CDC28 "Start" Cyclin Dependent Kinase. My initial work on temperature-sensitive mutants had been motivated by an interest in cancer with the hope of learning about the genes that controlled cell division. The genes we discovered, especially CDC28 seemed like they might eventually shed some light on why cancer cells divided. When Steve Reed joined the lab as a postdoc, he decided to focus on the CDC28 gene, setting up selections that uncovered new alleles as well as new genes that arrested at the same step. In 1980 he and Kim Nasmyth used recently developed techniques to clone the CDC28 gene (19) and after Steve set up his own laboratory, he found that it had protein kinase activity.