You still don't understand. I said the conclusions of the article are based on the fallacy of Affirming the Consequent. That does not mean that the actual science they did in identifying mutation hot spots and conserved areas was wrong, just that the conclusion that 'evolution' did this are based on a fallacy. Based on what I had already posted about methylation and error-correction schemes at the cellular-level I was only showing that mutation is not 'random'. For mutation to be 'random' and your objection to make sense, I would have to accept the fallacy of Affirming the Consequent, which I don't. Different thing altogether.
"Gene activity doesn't mean mutation."
One of the functions of methylation is to identify mutations for repair. You said this yourself and now pretend it doesn't exist so you can try to make a point.
"Constraint of expression doesn't mean constraint of mutation."
Again, you omit the role that methylation has no role in DNA repair which does relate to mutation.
To return to the initial problem. This was all done to show that your statement about mutation being 'random' was wrong. We now know that when you say 'random', you mean probabilistic.
The “work” they did to identify hot spots was an ASSUMPTION on their part that the differences in the eleven species they compared’s p53 molecule was due to MUTATION in a COMMON ANCESTOR. The “work” was a comparison of the DNA sequence AS IT EXISTS in eleven different species.
If one assumes those eleven species never HAD a common ancestor (as I assume you do) then the comparison of p53 was comparing God's design of p53 in eleven different species and figuring out which amino acids were essential to p53 function and which God would change or allow to change.
Do you FINALLY get it through your head that they didn't actually test mutation, they assumed it based upon common ancestry. They compared DNA and the resulting Amino Acid sequence of p53 in eleven species, and assumed any changes were due to mutation; they did NOT subject this DNA sequence to mutation and compare the results.
Gene activity has nothing to do with mutation repair. That is the activity of DNA repair enzymes, not gene activity. And methylation is involved only so the enzyme can tell the newly synthesized unmethylated strand (the one it assumes has the mistake) from the old methylated strand (the one it will use to repair the mistake). Not all DNA mutation is capable of being repaired this way because sometimes DNA methylase gets to the new DNA strand before the repair enzyme can do its work. DNA repair is in no way absolute, it is once more probabilistic.
Moreover DNA repair is something that a bacteria under stress DOWN regulates. Why would a bacteria under stress upregulate error prone DNA polymerase and downregulate DNA repair? For a better survival advantage of course!
Now why would upregulating mutation and downregulating repair confer a survival advantage? What is the mechanism of this survival advantage other than increased genetic variation for selection to act upon?
The definition of random INCLUDES probabilistic. A card game is random, but drawing a royal flush is not as likely a hand as any other.
Besides, what is your big bugaboo with “random” or “probabilistic” anyway. Do you think God has no power over random or probabilistic outcomes?