What happened next? . . . A series of ordinary gene duplications, many millions of years ago, copied some of these serine proteases. One of these duplicate genes was then mistargeted to the bloodstream, where its protein product would have remained inactive until exposed to an activating tissue protease—which would happen only when a blood vessel was broken. From that point on, each and every refinement of this mechanism would be favored by natural selection. Where does the many-layered complexity of the system come from? Again, the answer is gene duplication. Once an extra copy of one of the clotting protease genes becomes available, natural selection will favor slight changes that might make it more likely to activate the existing protease. An extra level of control is thereby added, increasing the sensitivity of the cascade.
(Miller 1999, 156-157)
