TAB3 functions in the NF-kappaB signal transduction pathway. It and the similar and functionally redundant protein TAB2, form a ternary complex with the protein kinase TAK1 and either TRAF2 or TRAF6 in response to stimulation with the pro-inflammatory cytokines TNF or IL-1. Subsequent TAK1 kinase activity triggers a signaling cascade leading to activation of the NF-kappaB transcription factor. Recent experiments have shown that TAB2 and the related protein TAB3 constitutitvely interact with the autophagy mediator Beclin-1; upon induction of autophagy, these proteins dissociate from Beclin-1 and bind TAK1. Overexpression of TAB2 and TAB3 inhibit autophagy, while their depletion triggers it, sμggesting that TAB2 and TAB3 act as a control point for autophagy.