Summations Only

My telephone number is also a type of information.
Therefore my telephone number affects genomes.

You have no evidence - this means that there is no "But in practice...".

I am not making claims about empathy: YOU ARE YOU need to support YOUR claims.

You seem to be essentially making a philosophical claim that the apparent randomness is not truly fundamentally random, but since your hypothesis does not include any criteria on which the two could be told apart it is entirely worthless in scientific terms. Many creationists and IDists have a similar approach claiming that the apparent randomness of mutations serves to mask subtle interventions to direct evolution by the Intelligent Designer/ God.

Your theory should at least be able to explain the facts we do have and be able to make different predictions than that made by the current theory of evolution. For example, your theory should be able to explain why chimps and humans differ in some genes more than others, and be able to do so better than the current theory. So what should we see when comparing the human and chimps genomes, and what predictions does your theory make that the current theory does not?

I think you've misunderstood what science means by predictions.

Sure it can. For example, we could look at the LTR's of orthologous endogeneous retroviruses (ERV's).quote:
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Third, sequence divergence between the LTRs at the ends of a given provirus provides an important and unique source of phylogenetic information. The LTRs are created during reverse transcription to regenerate cis-acting elements required for integration and transcription. Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration, even if they differed in the precursor provirus (Fig. 1A). Over time, they will diverge in sequence because of substitutions, insertions, and deletions acquired during cellular DNA replication.
Just a moment...
--------------------------------------------------------------------------------So we can predict that an orthologous ERV that inserted into the common ancestor of humans and african green monkeys will have more divergent LTR's than an ERV that is only shared by humans and chimps. This is exactly what we see, and what is evidenced in the paper cited above.

What guided mutations? Evidence please.

Your theory is unfalsifiable. If a mutation is detrimental or neutral you claim it is a product of random mutations. If it is beneficial then you claim it is due to guided mutations even if it occurs through the same mechanisms as detrimental and neutral mutations. It is no different than watching John Smith win the lottery and then declaring the lottery was guided so that John Smith could win, and counting this as a prediction. Sorry, doesn't work that way.

It seems strange then that absolutely none of the evidence presented in favour of an actual mechanism for guided mutations seems to have been in the metazoa. The only putative mechanisms that been put forward, i.e. Wright's de-repression based system, only seem to work in the context of unicellular organisms and have no readily apparent way to apply to multicellular organisms where there is a separation of the germ line from the somatic cells.

And welcome back to evolutionary genetics 101! This is absolutely basic stuff Zi Ko, and if you aren't familiar with it then you just don't understand evolutionary theory at all.The simple answer is that the disparities are principally the result of natural selection.

but when you ask why there are differences in the divergences of different genes between chimps and humans then you make it very clear that you ignore it, meaning that you are ignoring one of the central features of evolutionary theory.

Why should random mutations themselves have a predictive value? Why should it concern you?

Random mutations occur, they generated functional diversity and natural selection acts upon that functional diversity so as to over time shape the genomes of a population

Luria and Delbruck Flucutaiton ExperimentLederbergs' Plate Replica Experiment

How is this done? What are the molecular mechanisms that are involved? How does one design and experiment to test this hypothesis?

I came across a paper recently and I find it hard to believe that it isn't one Zi Ko has brought to our attention. The paper is 'Neural Control of Gene Recruitment in Metazoans' by Nelson Cabej (2011) who also has a website http://www.epigeneticscomesofage.com .
It seems that Zi Ko and Dr. Cabej may be long lost soul mates.

The hypotheses that the papers tested through those experiments did have predictive value. Please read the Luria and Delbruck paper. They spell out numerous hypotheses that they test with those experiments, one of which is random mutagenesis.

How does the rate reducing mechanism know which mutations to fix and which to not fix?

But we can talk about the fact that the same mechanisms that produce beneficial mutations also produce neutral and detrimental mutations which is contrary to the hypothesis of guided mutations.

That is not a mechanism. That is make believe. A mechanism has evidence to back it up.

.So we can predict that an orthologous ERV that inserted into the common ancestor of humans and african green monkeys will have more divergent LTR's than an ERV that is only shared by humans and chimps. This is exactly what we see, and what is evidenced in the paper cited above.

What guided mutations? Evidence please.

Your theory is unfalsifiable. If a mutation is detrimental or neutral you claim it is a product of random mutations. If it is beneficial then you claim it is due to guided mutations even if it occurs through the same mechanisms as detrimental and neutral mutations. It is no different than watching John Smith win the lottery and then declaring the lottery was guided so that John Smith could win, and counting this as a prediction. Sorry, doesn't work that way.