No, I have had to do two things to clarify things, defining science and evolution are the first fundamental step. That's pretty much been taken care of which is progress, great progress actually since I'm dealing with mostly trollers bent on repeating themselves endlessly. The philosophy of natural history known as Darwinism has been defined as well and I even managed to disentangle the equivocation fallacy of Darwinism and the theory of evolution.
We're on topic, as a matter of fact I think it's going way better then usual. You guys are only using two maybe three fallacies so it's easy enough to guide around that foolishness. I think I'm ready to start introducing evidence but it would probably be a good idea to give you guys some pointers on genetics. If your as woefully misinformed on Mendelian Genetics as you have been on the other background issues that could take a while.
Let's see, you probably know nothing about mutations, so why don't you check this page out:
In the living cell,
DNA undergoes frequent chemical change, especially when it is being
replicated (in S phase of the eukaryotic
cell cycle). Most of these changes are quickly repaired. Those that are not result in a mutation. Thus,
mutation is a failure of DNA repair. (
Mutations)
It's a little soon in the discussion but you really should try to get through this one:
When you think your focused enough this is the most comprehensive comparative genomics study I know of:
By comparing the whole sequence with the human counterpart, chromosome 21, we found that 1.44% of the chromosome consists of single-base substitutions in addition to nearly 68,000 insertions or deletions. These differences are sufficient to generate changes in most of the proteins. Indeed, 83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level.
(DNA sequence and comparative analysis of chimpanzee chromosome 22)
Then you need to know something about adaptive evolution in action.
The novel portion of the AFGP gene (encoding the ice-binding function) derives from the recruitment and iteration of a small region spanning the boundary between the first intron and second exon of the trypsinogen gene (Fig. 1). This newborn segment was expanded and then iteratively duplicated (perhaps by replication slippage or unequal crossing-over) to produce 41 tandemly repeated segments.(Origin of antifreeze protein genes: A cool tale in molecular evolution)
Ok so I'm tired of chasing your pitifully pedantic trolling tactics in circles, so the core terminology is defined and now it's time to get acquainted with the relevant source material. Just in case you don't realize by now I am well acquainted with the material. Now if you think you can keep up without actually reading it your going to find out the hard way I know exactly what I'm doing. I'll give you guys a couple of days to ponder some of that and I'll be back to see if you actually have the courage of your convictions. I'd be shocked if you did, I mean it would make you the first in a very long time.
Have a nice day 
Mark