The Spindle Assembly Checkpoint (SAC) delays the onset of anaphase until every chromosome is properly bioriented at the spindle equator. Mutations in SAC genes have been found in tumors and compromised SAC function can increase the incidence of some carcinomas in mice, providing further links between cancer etiology, chromosome segregation defects and aneuploidy. Here we review recent developments in our understanding of SAC control with particular emphasis on the role of the kinetochore, the nature of the tension sensing mechanism and the possibility that the SAC encompasses more than just stabilization of securin and/or cyclin-B via inhibition of the APC/C to delay anaphase initiation. Our primary emphasis is on the SAC in the budding yeast Saccharomyces cerevisiae. However, relevant findings in other cells are also discussed to highlight the generally conserved nature of SAC signaling mechanisms.