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This simple succession of events became complicated, however,
when it was discovered that Ras did not solely interact with Raf
but with at least eight other effectors involved in several cascades
activating many transcription factors. Because of these multiple
activations, the Ras protein has pleiotropic effects, and its action
on cell multiplication is a much more complicated process which
must depend on precise equilibrium between all these effects
(Campbell et al ., 1998). It has to be acknowledged, therefore, that
the initial explanation is no longer adequate, and a new, very diffi-
cult question arises from this example: if cell functions depend on
equilibrium between the activity of several signalling pathways, how
is this equilibrium controlled differentially and specifically in the
different types of cell in order for them not to perform the same
functions? We have to depart, in fact, from the initial theoretical
context based on specificity. The necessity for this can be demon-
strated with a little simple calculation. Let us take the one we did
in section 4.1.5 of this chapter, but instead of considering a cascade
of 20 interactions produced in an overall cell network, let us simply
take a cascade of four interactions, which would describe a sig-
nalling pathway from the initial protein signal to its target. This is
a sensible size of cascade for doing our calculation although in cer-
tain cases real cascades may be longer. At each step in the cascade,
there are again seven interaction possibilities with different proteins
for each protein. In this case, the combination possibilities are such
that the signal may activate (or repress) 2401 different targets. If
there is one more step in the cascade, this number rises to 16 807.
If the cascade involves six interactions, which is still a reasonable
number in view of the size of actual cascades, we are faced with
117 649 potential interactions. How, from the point of view of deter-
ministic functioning based on stereospecificity, is the signal going to
be directed to its specific target among these thousands of poten-
tial interactions? One answer is to say that there is a set of molec-
ular targets for each signal and that this set is what is specific to
the signal. Yet this answer does not hold water either. Let us go
back to our calculation. In a mammal there are about 250 different
types of cells. According to the theory of genetic programming, at
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