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in the sense that the cells will not grow as healthy compared to a variant that is coming from a near evolutionary distance.

Because we see translation machinery as almost, it is so conserved and so essential.

It is not even clear whether we can remove some of the parts or whether the entire translation will need all of the same parts in the same efficiency.

We don't understand the rules of this machinery.

So the first thing we all understand is that what is the resilience?

What are we really talking about here when we talk about you cannot mess with this translation?

Is this true?

Because it is so conserved and so similar and functions in the most conserved ways, that was the first thing that we wanted to understand.

No, I wouldn't say that.

In the biological level, yes, because we found that the...

different modules started responding to the changes that we've introduced and that we could never recover the translation as effectively as it used to be.

So that it never reached to its optimality, that it was always suboptimal.

It needed, say, one more mutation perhaps to get there.

It accumulated four mutations.

We did a lot of experiments to understand this, of course.

It was accumulating mutations.

It was getting better at its task.

Maybe it needed a couple other mutations to get really good at it, but somehow those mutations never happened.

And before those mutations happened, we saw another module emerging through mutations and getting better at its own different task that is not translation.

You can think of cell as a web of networks, right?