I think you need to do some research and look at the actual evidence.
…he wrote, while running away from looking at the actual evidence. 
What does the existence of 4500 known variants tell us? Big picture, please, using only words with agreed-upon definitions. You can’t do it.
As the last two exchanges show, this doesn’t work, since you “clarify” your gibberish with additional gibberish, and understanding is not thereby advanced. Note that @Mercer doesn’t understand what you’re trying to say either.
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And it’s a twofer, as its very existence falsifies Behe’s claim that HIV has evolved no new proteins or binding sites since it entered humans (Edge of Evolution, p. 143-4).
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John can speak for himself but based on his comment he understands. What he needs to do is some research comparing different proteins to see that his argument is not on solid ground.
Then why did he say this?:
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LMAO
Hilarious. Bill starts with an invalid inference with a wrong conclusion, then using this a premise derives a true statement from it (it is true that “it does not indicate how many substitutions will be conserved in the population over time”) through a complete non-sequitur.
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You don’t have the slightest idea what I’m talking about, so you can’t have the slightest idea whether what I’m saying is on solid ground or not.
Articulate a hypothesis, Bill. Not an argument. Not a claim. Not word salad. Not a vague, incoherent question like:
How did the change happen given known evolutionary mechanisms and become fixed in the human population?
Try to use words that professionals use, like ortholog, homolog, allele, and residue.
And try to keep the nested hierarchy in mind, as your question quoted above seems to be suggesting that we think that human NOTCH2 is a direct descendant of murine Notch2.
At this point it tells us that there are around 1 to 3 AA changes per protein amino acid position that can be tolerated in the human population.
I think in this case you are mistaken. It does not mean what you think it does as other proteins have lots of variation in the human population but almost no changes between species. How do you explain this?
You’ve already done that. You’re just restating the observation in more general terms.
How does this evidence relate to your incoherent question quoted above?
And
does not meet my semantic requirement.
You seem to think that your redundancy and neologisms make what you write seem more formal. They don’t.
I’m not.
I think that you have no idea what I, or anyone else, think, given your inability to communicate or understand written English.
Easily. You are failing to grasp the obvious fact that we know much more about human variants because we have looked so much harder in humans for them.
I can’t see how even a layperson could miss something that obvious. I explicitly pointed this out and patiently explained this to you above, but you did not respond:
What’s your excuse for ignoring this, Bill?
I will try to speak in the professional language.
This is the substance of what we are discussing.
Do 4500 observed residue substitutions support that the differences we see between mice and humans are due to mutations or different starting points?
The number 4500 known human variants in Notch 2 does not strongly correlate with how many sequence variants we are seeing between mice and humans.
You’re failing already with “variants” at the end.
No, it is not. The substance is that you hypothesize that known mechanisms of genetic variation are insufficient to explain genetic differences between mice and humans.
It’s ludicrous. I am simply falsifying your hypothesis by showing you the massive intraspecies variation in humans for a gene you chose.
If you were sincere about looking for truth instead of debating, you’d maybe do some math, extrapolating from the relevant times (130 million years for mice and humans from a common ancestor), to confirm that your hypothesis has been falsified, but math really isn’t needed–it’s that obvious.
Yes. They demolish your hypothesis, which you are afraid to state as a hypothesis.
More word salad. In genetics, “variants” does not generally refer to differences between species.
You’re not seeing very well.
How much variation is there in mice? Would the variants identified to date in COMPLETELY INBRED strains of house mice be comparable to what we have learned to date from clinical genetics?
A lot of science is keeping track of what we know and what we don’t.
In order for your claim of falsification to be correct you need to show correlation between residue substitutions in human populations with residue substitutions in mice. The proteins we have discussed are myosin 7 and notch 2. Both have thousands of substitutions does that correlate with the differences in mice and human residues?
The answer is no. myosin 7 has 1935 amino acids it has 3154 substitutions. Humans sequence similarity to mice: is around 97.5%
notch 2 has 2471 residues and its number of variants in humans is 4805. Humans sequence similarity to mice: is around 92.5%
3x (7.5% vs 2.5%) the percentage of residue substitutions between humans and mice yet only 30% larger percentage substitutions in humans.
No, I just tried to explain this to you in detail.
We’ve sampled much more of the human population than we have of the mouse population, so we don’t know how much polymorphism there is in mice.
Your recitations are meaningless.
How would the number of polymorphisms mice help with the analysis?
Why did you write:
???
The subject has been residue substitutions in the human population vs residue substitutions between humans and mice.
I should have spelled that out better.
No, the subject is your hypothesis that existing mechanisms cannot explain the differences between human and murine Notch2.
So in humans, we have less than a million years. For humans and mice, we have 130 million years.
Where did the human polymorphisms come from?
In the case of the human population mutations. In the case of the human and mice consensus sequences it may be due to different starting points.