The cell cycle is a ubiquitous and intricate process that takes place in a cell leading to the engenderment of two daughter cells. Precise regulation of this process is indispensable to ascertain the genetic integrity of a cell. Cyclins and cyclin-dependent kinases are central to this cycle. Cell cycle progression is withal controlled by negative regulatory proteins, including INK4, Kip/Cip, p53, and Rb. Loss of cell cycle control is a hallmark of cancer, and cell cycle regulation has been a profound research subject for two decenniums. Besides cancer, hundreds of xenobiotics are kenned to influence cell cycle-cognate events causing cell injury and cell death. It has been established that both carcinogenic and non-carcinogenic toxicants can considerably alter cell cycle concrete events. Many of the drug- or chemical-induced alterations are reversible and many are irreversible; it all depends whether the cell cycle regulatory events are altered of influenced by parent compounds, their metabolites, or their biological reactive intermediates. Overall, it seems likely that micromanaging cell cycle events may have a tremendous therapeutic value. The events of the cell cycle are masterpieces of molecular engineering, employing distinct machineries (such as DNA polymerases for replication, the microtubule spindle for segregation, and actin and myosin fibers for cytokinesis) to engender two cells from one. These machineries are governed by a biochemical clock that is in turn controlled by exquisitely tuned signaling pathways processing information from both inside and outside the cell to ascertain the correct order of events and to sanction proliferation only when it is congruous for the organism. Derangements of cell cycle control pathways by mutations in somatic cells make a paramount contribution to disease, and in particular to cancer. Mutations that uncouple cell cycle progression from its mundane requisite for hormones or anchorage cause uncontrolled proliferation, while mutations that cripple checkpoint controls can cause cells with damaged DNA to proceed with DNA replication or cells with unattached chromosomes to proceed through chromosome segregation, dramatically expediting the rate at which the cells acquire more mutations, and incrementing the chance that they will become malignant.