In multicellular eukaryotic systems, both leukocytes and certain tumor cells have been observed to move in an amoeboid fashion, distinct from that of mesenchymal migration . These movements are generated by cortical actin and driven by weak and short-lived interactions with the substrate [7,8]. Some cancers preferentially use this type of motility to avoid the requirement for extracellular matrix (ECM) proteolysis  and escape tissue barriers .
Blebbing motility has also been observed in a variety of other cell types and model organisms, including fish embryonic cells [10, 3], primordial germ cells (PGCs) in zebrafish  and Drosophila melanogaster embryos .
Although blebbing is now known to be a mode of migration, much of the initial findings on the mechanics of blebbing comes from non-migratory cells. Subsequent studies suggest similar mechanisms are likely to be used by migratory cells. In both cases, the blebbing cycle can be simplified into 3 major steps, namely initiation, expansion and retraction .