In the DNA code list, that critical information is contained in a short stretch of As and Cs and Gs and Ts that lie just before each gene and act as a switch that turns the gene on or off. The switch, in turn, is flicked on by proteins called transcription factors, which activate certain genes in response to certain stimuli. Naturally, every gene is not regulated by its own distinct transcription factor; otherwise, a codebook of as many as 30,000 genes would require 30,000 transcription factors—and 30,000 more genes to code for them. Instead, one transcription factor can flick on an array of functionally related genes. For example, a certain type of injury can activate one transcription factor that turns on a bunch of genes in your white blood cells, triggering inflammation.

Accurate switch flickers are essential. Imagine the consequences if some of those piddly nucleotide changes arose in a protein that happened to be a transcription factor: Suddenly, instead of activating 23 different genes, the protein might charge up 21 or 25 of them—or it might turn on the usual 23 but in different ratios than normal. Suddenly, one minor nucleotide difference would be amplified across a network of gene differences. (And imagine the ramifications if the altered proteins are transcription factors that activate the genes coding for still other transcription factors!) When the chimp and human genomes are compared, some of the clearest cases of nucleotide differences are found in genes coding for transcription factors. Those cases are few, but they have far-ranging implications.

The genomes of chimps and humans reveal a history of other kinds of differences as well. Instead of a simple mutation, in which a single nucleotide is copied incorrectly, consider an insertion mutation, where an extra A, C, G, or T is dropped in, or a deletion mutation, whereby a nucleotide drops out. Insertion or deletion mutations can have major consequences: Imagine the deletion mutation that turns the sentence "I'll have the mousse for dessert" into "I'll have the mouse for dessert," or the insertion mutation implicit in "She turned me down for a date after I asked her to go boweling with me." Sometimes, more than a single nucleotide is involved; whole stretches of a gene may be dropped or added. In extreme cases, entire genes may be deleted or added.

More important than how the genetic changes arise—by insertion, deletion, or straight mutation—is where in the genome they occur. Keep in mind that, for these genetic changes to persist from generation to generation, they must convey some evolutionary advantage. When one examines the 2 percent difference between humans and chimps, the genes in question turn out to be evolutionarily important, if banal. For example, chimps have a great many more genes related to olfaction than we do; they've got a better sense of smell because we've lost many of those genes. The 2 percent distinction also involves an unusually large fraction of genes related to the immune system, parasite vulnerability, and infectious diseases: Chimps are resistant to malaria, and we aren't; we handle tuberculosis better than they do. Another important fraction of that 2 percent involves genes related to reproduction—the sorts of anatomical differences that split a species in two and keep them from interbreeding.

That all makes sense. Still, chimps and humans have very different brains. So which are the brain-specific genes that have evolved in very different directions in the two species? It turns out that there are hardly any that fit that bill. This, too, makes a great deal of sense. Examine a neuron from a human brain under a microscope, then do the same with a neuron from the brain of a chimp, a rat, a frog, or a sea slug. The neurons all look the same: fibrous dendrites at one end, an axonal cable at the other. They all run on the same basic mechanism: channels and pumps that move sodium, potassium, and calcium around, triggering a wave of excitation called an action potential. They all have a similar complement of neurotransmitters: serotonin, dopamine, glutamate, and so on. They're all the same basic building blocks.

The main difference is in the sheer number of neurons. The human brain has 100 million times the number of neurons a sea slug's brain has. Where do those differences in quantity come from? At some point in their development, all embryos—whether human, chimp, rat, frog, or slug—must have a single first cell committed toward generating neurons. That cell divides and gives rise to 2 cells; those divide into 4, then 8, then 16. After a dozen rounds of cell division, you've got roughly enough neurons to run a slug. Go another 25 rounds or so and you've got a human brain. Stop a couple of rounds short of that and, at about one-third the size of a human brain, you've got one for a chimp. Vastly different outcomes, but relatively few genes regulate the number of rounds of cell division in the nervous system before calling a halt. And it's precisely some of those genes, the ones involved in neural development, that appear on the list of differences between the chimp and human genomes.

That's it; that's the 2 percent solution. What's shocking is the simplicity of it. Humans, to be human, don't need to have evolved unique genes that code for entirely novel types of neurons or neurotransmitters, or a more complex hippocampus (with resulting improvements in memory), or a more complex frontal cortex (from which we gain the ability to postpone gratification). Instead, our braininess as a species arises from having humongous numbers of just a few types of off-the-rack neurons and from the exponentially greater number of interactions between them. The difference is sheer quantity: Qualitative distinctions emerge from large numbers. Genes may have something to do with that quantity, and thus with the complexity of the quality that emerges. Yet no gene or genome can ever tell us what sorts of qualities those will be. Remember that when you and the chimp are eyeball to eyeball, trying to make sense of why the other seems vaguely familiar.