The fix Was InWhen evolutionists found out that the chimp and human genomes were practically identical they went ape, claiming the evidence all but proved our shared lineage, with the chimp, to a small, primitive, ancestral primate. There was only one problem: With so few random genetic changes, how would such dramatic and complex changes come about? Far from a confirmation, our similar genes posed a dilemma for evolution. For how could so little genetic change cause so much significant evolutionary distance be traversed? And if the answer is, as it always seems to be, that those rare and random genetic changes were able to achieve such monumental results because the requisite parts and pieces that would be used were, fortuitously, already in place (because they just happened to have evolved for some other reason), then we have entered the realm of just-so stories. For the theory then amounts to the claim that “the fix was in.” The various key ingredients to making a human were all there, lying around, perhaps in disguise, or perhaps doing some other job. And then they were systematically recruited, coming into their own by virtue of a few, rare, mutations finally occurring and enabling the puzzle pieces to come together. It would be like a supersonic jet aircraft just happening to come together because its various parts just luckily were lying around. That is serendipity on steroids.
Well it just gets worse. More recently evolutionists were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.”
In fact the beneficial mutations in protein-coding genes, which presumably would be important in evolving the human from a small, primitive ape, literally number only in the hundreds. It would be astonishing if the human could be evolved from so few mutations.
But again, it just gets worse. For now evolutionists must conclude that not only are there few random mutations that must somehow create Newton and Einstein (to name just a couple of humans), and not only are most of those mutations neutral or slightly deleterious, and not only would evolution probably have only a few hundred genes undergoing selection, but that a monumental part of that evolutionary change, so important in creating humans, must have arisen from, yes, a single mutation. To wit:
What distinguishes humans from monkeys and apes? The gene ARHGAP11B is probably among the things that make humans special: This gene is only present in humans and contributes to the amplification of brain stem cells. Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden have now made a spectacular finding: It is a single base pair substitution in the ARHGAP11B gene that ultimately is responsible for the ability of the ARHGAP11B protein to amplify brain stem cells, a process thought to underlie the expansion of the neocortex in modern humans.
Spectacular indeed. As one of the researchers explained:
This change is tiny on a genomic scale but substantial in its functional and evolutionary consequences – it’s a single base substitution that likely drove brain size evolution and that may have set the stage for what makes humans special.
A single mutation? Here we have evolution reductio ad absurdum. A single mutation essentially worked the magic to create humans. How lucky we are.
Of course such absurdity entails the idea that an army of molecular components were serendipitously in place, ready and waiting for the single mutation to unleash their creative powers.
The fix was in.