Okay, I am actually the one to blame for people thinking that the neural crest genetic variant medical disorder ferrets get is WS, and I guess that was something like 15 years ago. Since then a classical geneticist who looked into it has noted that while some may have their markings due to WS it is more likely that the neural crest genetic variant, KIT oncogene is to blame. One reason for saying so is because of the body spotting/ body splotching also seen. Since that has been mentioned for years I hope more sites catch up. That's not good news, actually. Oncogenes can increase the malignancy risk for an individual. There are other risks as well. To understand what is going on you need to know about fetal development. This, BTW, relates to why the cells usually needed for stem cell research are NOT from adults, nor from developed fetuses but from blastulas. The blastula is an early fetal stage when there is just a hollow ball of cells. There are no organs, there are no senses, there are no features. In fact, what these are are the extra 8 day old fetal stage which is used to impregnate women who are having fertility problems. Using the extras for stem cell research advances medical knowledge while keeping a number of these from being thrown away as medical waste. But, I am getting off the point slightly. The reason these cells are so useful for stem cell research is because any tissue type would later derive from them. That point is essential for understanding neural crest discussions. You see, as time goes on, the fetus develops cell regions which are more specialized so they have fewer types of cells they will later develop into. After a while one of these regions is the cardiac neural crest. Later the cardiac crest which is responsible for things like cardiac and some major vascular development separates from the neural crest which provides head pigmentation, some ear structures, some intestinal structures, some mandibular development, etc. Now, if the mutation is for the cardiac neural crest cells then any of the tissues which develop from this early fetal region MAY be affected. Note that I say, "may". These fetal cell genetic medical disorders have what is called "variable expression". That means that a person can have a ferret parent who has a mild presentation but the offspring might be severely affected. This is why there is a higher rate of certain cardiovascular problems, including both cardiomyopathy types, but especially the harder to find (before death) hypertrophic cardiomyopathy. (You can find some articles on this in the archives of Ferret-Genetics in Yahoogroups and elsewhere.) Some of these circulatory problems result in small litters due to reabsorbed dead fetuses, or litters with a number of members who die soon after birth due to increasing the circulatory malformation fetal death rate. There can also be a higher newborn death rate due to deaf ferret mothers not getting all of the signals they need for rapid and correct responses. Multiple breeders have discussed encountering these problems, and there is a lot in the literature on this in an assortment of mammals. More commonly, the problem seems to be mutations affecting the neural crest segment of cells after that splits from the cardiac crest. These can carry medical concerns for intestinal development, ear development, mandibular (jaw) development, etc. All of this may explain why it appears that ferrets with these genetics tend to less commonly live to a previously very normal age of older than late in the 6th year, and why it is important to start old age exams for them earlier than you would for others. These genetics were RARE in the U.S. a couple of decades ago and the lifespans commonly seen were better, too. Now-a-days, especially from a number of ferret farms (although the push for these fancies first came from private breeders and one mid-sized farm, many of which charged extra for the marked kits) it is rare to encounter a ferret who does not have extraneous white splotches such as panda heads, head blazes, body spotting, or incomplete mitts or incomplete bibs. All such markings are neural crest variant markings. The body markings are especially inclined to be KIT oncogene ones. (WS in mammals can cause the head markings but does not tend to cause the body markings.) Right now breeders elsewhere have a window in which they can educate and reduce the breeding for these "fancies" to avoid the genetic time-bomb seem too often here. Such markings are present THROUGHOUT life rather than being roaning (lightening which happens later in life). BTW, I have found myself wondering after many discussions if knee patches may at times have a different genetic cause. Complete and cleanly margined bibs seen with complete mitts (cleanly margined, full socks) in which those normal dark portions on a standard are entirely de-pigmented DO have a different genetic cause and that cause has never been associated with any medical problems. That is safe. It is one reason shows should separate the types in judging. See the FML Archives (addy in the header of each day's FML), the FHL Archives <http://fhl.sonic-weasel.org>, and Ferret-Genetics Archives <http://groups.yahoo.com/group/Ferret-Genetics/> [Posted in FML issue 4833]