Blebs are protrusions of the cell membrane. They are the result of actomyosin contractions of the cortex, which cause either transient detachment of the cell membrane from the actin cortex or a rupture in the actin cortex. Then, cytosol streams out of the cell body and inflates the newly formed bleb. During expansion, which lasts approximately 30 s, the bleb is devoid of actin and the surface area increases through further tearing of membrane from the cortex and convective flows of lipids in the plane of the membrane through the bleb neck. Once expansion slows, an actin cortex is reconstituted. First actin-membrane linker proteins, such as ezrin, are recruited to the bleb, then actin, actin-bundling proteins and finally myosin motor proteins. Retraction lasts approximately 2 min and is powered by myosin motor proteins. Though it has been less studied than other actin-based membrane protrusions such as lamellipodia or filopodia, blebbing is a common feature of cell physiology during cell movement, cytokinesis, cell spreading and apoptosis. This review will succinctly attempt to summarize what we know about the mechanisms involved in blebbing, when it appears in cell physiology and what open questions remain.