The fact is, genome project or not, we do not know how many genes or proteins are in humans. And the old adage that one gene = one protein is still pretty much true. When two different products come off a single gene, we call them isoforms--but still consider them the same protein. The genome project had absolutely no bearing on what we know of genetic complexity; it merely gave us the sequence for the entire genome, so that it is now in searchable databases. I have even made use of that information.
In any case, the whole complexity of the genome (human or otherwise) pretty much supports the theory of evolution. From the creationist standpoint, there is absolutely no reason for the hundreds of duplicated DNA elements in the genome... no reason for pseudogenes, which code for proteins that aren't even made, yet still exist in the genome like so much excess weight... etc. It really looks like the result of mindless mixing, and not like the product of intelligent design.
Several months ago I brought up the fact that there is a shared mutation that prevents people, chimps, gorillas, et al from producing vitamin C. I can't remember which C used which speculation to avoid the obvious conclusion, but I do remember one of 'em saying that it's a sign the designer used common parts, rather like a car manufacturer, and (I'm not kidding) another one proposing research into why ape DNA is more vulnerable to mutation than monkey DNA!
I have no problem with that, thanks for the warning!
The fact is, genome project or not, we do not know how many genes or proteins are in humans. And the old adage that one gene = one protein is still pretty much true. When two different products come off a single gene, we call them isoforms--but still consider them the same protein.
While it is true that they are called isoforms, and that obviously they share much the same amino acid sequence, does not mean that this is not an extremely important discovery. It is also a fact that these different proteins are indeed necessary:
In vertebrates, the four A-actin isoforms present in various muscle cells and the B- and Y-actin isoforms present in nonmuscle cells differ at only four or five positions. Although these differences among isoforms seem minor, the isoforms have different functions: A-Actin is associated with contractile structures, and B-actin is at the front of the cell where actin filaments polymerize. From: The Actin Cytoskeleton
In this case the different forms have very important functions. So there is a need for this highly complicated system of alternative gene splicing.
This presents many problems to evolutionary theory of course. The change in one gene can affect several functions for one thing, it is hardly likely that it would be beneficial to all the gene's functions. Furthermore the existence of such multi-purpose genes makes it very unlikely that they could have arisen by random evolutionary means.
The further problem these multi-purpose genes show is that not only do many genes require a system to initiate, regulate, and stop protein production, but that they also need a system to tell them how to make different proteins. Surely developing such an intricate system is not the result of random chance. Surely, such a system is irreducibly complex and a sign of intelligent design.