Not in the slightest. First of all Doolittle never claims that the mice were completely without issue as Behe appears to suggest. What he wrote is:
Let me conclude by mentioning that support for the Yin and Yang scenario is now coming from another quarter. Thus, it has become possible during the last decade to “knock out” genes in experimental organisms. “Knockout mice” are now a common (but expensive) tool in the armamentarium of those scientists anxious to cure the world’s ills. Recently the gene for plaminogen was knocked out of mice, and, predictably, those mice had thrombotic complications because fibrin clots could not be cleared away. Not long after that, the same workers knocked out the gene for fibrinogen in another line of mice. Again, predictably, these mice were ailing, although in this case hemorrhage was the problem. And what do you think happened when these two lines of mice were crossed? For all practical purposes, the mice lacking both genes were normal
Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. Music and harmony can arise from a smaller orchestra. No one doubts that mice deprived of these two genes would be compromised in the wild, but the mere fact that they appear normal in the laboratory setting is a striking example of the point and counterpoint, step-by-step scenario in reverse!
And the authors Bugge et al do state in their paper:
“Remarkably, mice with each of these deficits, even in combination, were born normal in appearance, survived to adulthood, and produced offspring. Thus, the major components of the PA-Plg system are not strictly required for development, growth, and reproduction.”
And later:
Fib Deficiency Alleviates Wasting of Plg-Deficient Mice
To examine the role of single and combined deficiencies in overall growth and survival of the mice, we followed the fate of a prospective cohort of mice initially consisting of 44 control mice, 25 Plg−/− mice, 16 Fib−/− mice, and 23 Plg−/−/Fib−/− mice. Plg−/− mice had essentially normal weight gain until 2 months of age (Figure 1b). Thereafter, a progressive weight loss was observed, which became severe after 4 months. The weight of Plg−/− mice 6 months or older was uniformly less than two-thirds that of control mice (Figure 1a and Figure 1b). In contrast, mice lacking only Fib exhibited normal weight gain as adolescents and no wasting phenomenon as adults, even when followed for more than 12 months (Figure 1a and Figure 1b). Remarkably, in the same genetic background, Plg−/−/Fib−/− mice, despite their lifelong lack of Plg, exhibited the same excellent growth properties as those of control and Fib−/− mice (Figure 1a and Figure 1b). Indeed, no signs of weight loss or wasting were observed in any of more than 20 Plg−/−/Fib−/− mice that were followed for more than a year. This dramatic rescue from the severe-wasting syndrome normally associated with Plg deficiency provided a first indication that general ill health in young Plg−/− mice depended on fibrin(ogen).
And of course we do have to consider that these genes didn’t evolve in mice, which ultimately can’t substitute well for the ancestral state even with gene knockouts, in the evolutionary history of the blood clotting cascade. So the fact that the loss of these genes in a modern context still incurs various health or fitness penalties doesn’t tell us that the ancestral state would be an unviable organism, nor that natural selection wouldn’t favor the gains of these two genes in the ancestral background.
It’s not clear how I am supposed to take this as a misreading by Doolittle, much less a problem for the evolutionary scenario for the blood clotting cascade.