There KIT oncogene tends to be dominant, but remember that dominance depends on the RELATIONSHIP BETWEEN TWO ALLELES, so it entirely possible for an allele to be dominant to something and recessive to something else, just as a person may exert power over one individual but take orders from another one. Some are strongly dominant, some strongly recessive, but it always depends on what combination the individual inherits. To top it off sometimes there are variations of some alleles, and sometimes the expression is very dependent on the actions of alleles in other genetic locations which may either supress or enhance their actions. Sometimes even environmental factors play in. A family which is normally quite resistant to malignancies may still wind up with them if smoking or eating a lot of animal fat is common. A child who was undernourished when young may have the genotype (the genetic alleles) for being tall but will wind up stunted, so that individual has a tall genotype but wound up with a short phenotype. You can think of enough examples to fill a page, I would suspect. Remember, too, that some genetic messes are a LOT harder to get out of then they were to get into. This is one of them. It is better avoided in nations where people are intelligent enough to learn through reading rather than through experience trouble first hand. An example of studies on KIT oncogene which mention dominance (and there are a lot): Development. 1996 Nov;122(11):3597-605. The dominant white spotting oncogene allele Kit(W-42J) exacerbates XY(DOM) sex reversal. Nagamine CM, Carlisle C. but then also consider: : Genes Cells. 1998 Apr;3(4):235-44. recessive spotting: a linked locus that interacts with W/Kit but is not allelic. Bennett DC, Trayner ID, Piao X, Easty DJ, Kluppel M, Alexander WS, Wagner EF, Bernstein A. BACKGROUND: The murine coat-colour mutation recessive spotting (rs) maps very closely to the W/Kit locus, encoding the proto-oncoprotein Kit, the protein tyrosine kinase receptor for stem cell factor. Kit is important in the development of melanocytes, germ cells, interstitial cells of Cajal (ICC) and haemopoietic lineages, including mast cells. rs has never been genetically separated from Kit, and interacts with Kit mutations, suggesting that it is a recessive allele of Kit. Here we have tested this possibility... so as you can see there are not only relationships to consider but also variations of the alleles. The concept of variable expression is essential to understanding neural crest genetics and why it will be so hard to reduce the proportion even though we should still try, and why nations where this morass has not yet been created the ferret clubs need to educate, educate, educate to stop people from breeding ferrets with such markings. It is harder to get out of this increase in the proportion of these alleles than it was to get into it. In variable expression the phenotype varies and the degree to which the allele expresses itself varies among individuals WHO HAVE THE EXACT SAME ALLELE. This is because the action of that genetic variant is on early fetal cells which have not yet differentiated. So, let's just take a situation in which the individuals have not inherited the alleles in multiple numbers, and has not inherited alleles at other loci (genetic locations) which also cause neural crest variations. Okay, one individual with the allele may have outward signs suppressed, another may have them show up in part or to some degree, yet a third may be suffering badly due to having a phenotype which expresses the neural crest variant genotype strongly. The kits of the first will NOT have any genetic benefit over the kits of the third. They have the allele, so a parent who looks okay can have offspring whose lives will pay badly for that allele. Then top it off with this bit of reality: our ferrets may be dealing with more than one type of neural crest genetic variant, and there are multiple loci (genetic locations) in which such mutations can cause neural crest medical disorders (for instance there are at least 5 ways to cause Waardensburg Syndrome in mammals). This means that a ferret can wind up with multiple neural crest causes which have been increased in the population through breeding for appearance. Having multiple causes in one individual may increase the phenotypic results, too. [Posted in FML issue 4670]