In summary, Vav-1 is irreplaceable for T cell function; however, it now looks like it is not critical for the initial stages of T cell interaction with an APC but is required in a more subtle way for the cell to correctly orientate towards an APC and form a productive T cell synapse. An interesting issue is how Vav-1 links to other molecules known to contribute to integrin activation and immune synapse formation. These include GTPases such as Rap1A and Cdc42, and adapter molecules like ADAP (also known as SLAP130 or fyb) [15-18]. Future questions about Vav-1 also relate to its potential to act independently of its capacity to activate Rac-1, 2. It has been shown that gain-of-function mutants of Rac-1 can rescue developmental defects caused by loss of Vav-1 in the thymus but the full actions of Vav-1 in the periphery have not been examined and the possibility that Vav-1 works as an adapter as well as a regulator of GTPases is an unresolved issue . However, what is now clear is that Vav-1 does not globally regulate the T cell cytoskeleton; rather it works as a component of a complex network of molecules which exist for this purpose.