Evolution of Poison

Well, it's not all that difficult. For example, one particular toxic component (seraphotoxin) in a snake venom is derived from a peptide hormone that regulates heart function in vertebrate animals (endothelin) . All these animal produce the hormone in minute amounts. However, if you get an overdose, it makes your heart fibrillate, which will kill you (Heart fibrillation is the condition which is treated with an electric shock to the chest in an emergency room). If, for example with the help of a so called transposable element (jumping gene), a copy of this gene was moved into the place of a gene for a protein produced in a salivary gland, this simple mutation would render the bite of the animal highly toxic, even without the complex poisen fang apparatus modern venomenous snakes possess. Since the toxin is a protein, it is only toxic when injected into the blood stream, in the digestive track it gets degraded. Thus one single mutation copying a gene into a different context on the chromosome gave it a different function, further evolution then refined the delivery process. Other components of snake venoms derive from other genes, which similarely have benign function in the snakes metabolism, but are toxic when injected into your bloodstream through a snake bite. That's an example of the process which kongstad meant with "gene recruitment". It did not need the slow evolution of a harmless protein to a toxin, the simple effect of overproducing a particular normal protein (a peptide hormone) in a particular place (the salivary gland), that is, to copy and paste a particular piece of DNA from one place into another, changed its function.