NFKB1 and viral infectious disease: While the outcome of this might be expected to be a re-focusing of the infected cell’s degradative capability to the poxviral targets, examples so far have indicated that targeted host proteins, which can act as control points in the anti-viral response (e.g., Akt in the cell-cycle and p105 in NF-κB regulation), are stabilised and protected from the degradation by cellular activity induced by viral infection, thereby maintaining the infected cell in a state conducive to viral replication.