How does an inhibition complex reactivate again for its own signal transduction. I am interested to know the possibilities of a kinetic mechanism of signaling cascade of inhibitory complex.

We generally know, that the inhibitors block the kinase sites to switch off particular complexs via structural change confirmations. Are there any alternative ways to gain the signal to follow its own mechanism?

Example: Inhibition of Nf kb kinase, as a secondary activation of TLR 4 by LPS could make any changes in inhibited kinase complex to gain the activation, subsequently to tranlocation and gene expression?