The redundancy of many cytokine functions that was first noted in vitr
o has now been confirmed in vivo with the demonstration that some of t
hese functions can occur in mice rendered deficient in a cytokine or c
ytokine receptor by gene inactivation. Other functions are ablated in
these mice, suggesting that they are cytokine-specific. Although some
of the underlying mechanisms have been identified, it remains unclear
why certain activities of a cytokine should be unique and others redun
dant. It is proposed that compensatory mechanisms exist only for those
cytokine functions whose inappropriate or excessive activation would
not be pathogenic or whose importance justifies this risk. Conversely,
cytokine-specific functions might be those that should be tightly reg
ulated to avoid the pathological consequences of their inadvertent exp
ression.